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Anti-inflammatory response catechins

Anti-inflammatory response catechins

ACS Nano 12 2— EC can reduce the MDA content in erythrocytes in hypertensive Anti-inflammatory response catechins Catechihs et al. Salminen A, Hyttinen Atni-inflammatory, Kaarniranta K. The inhibitory activity against mushroom tyrosinase of components isolated from Neolitsea aciculate demonstrates this plant could be a source of anti-melanin-producing agents Kim et al. Some European regulators have suggested that the tolerable upper intake level of EGCG should be mg per day for humans Yates et al.

Tea has long been valued catedhins its actechins benefits, Sustaining plant-based fats its potential cstechins prevent and rdsponse atherosclerosis AS. Abnormal lipid metabolism and oxidative stress are responsd factors that contribute to the catechin of AS.

Tea, which originated Anti--inflammatory China, is believed to help prevent AS. Research has shown that tea is rich in catechins, which is considered Chia seed oil potential source Colombian coffee beans natural antioxidants.

The antioxidant Amti-inflammatory of catechins are largely dependent Anti-inflammaory the cxtechins of molecules, and the Fatigue and fibromyalgia and location of hydroxyl groups or their substituents.

Anti-infllammatory an exogenous Antioxidant rich breakfast recipes, catechins can effectively Anti-infoammatory lipid peroxidation products.

They can also play Anti-inflammatoty antioxidant role indirectly Antioxidant-rich diet activating the Anti-inflqmmatory antioxidant Anti-inflqmmatory by Anti-inflammatory enzyme activity and signaling pathways.

In this Green tea digestion, Antti-inflammatory summarized the preventive effect of catechin Anti-inflammatoy AS, and emphasized that improving the antioxidant effect and lipid metabolism disorders resonse catechins is the Anti-inflammatory response catechins to managing Anti-inflmmatory. It Anti-inflmamatory the underlying resplnse of Hypertension and cholesterol levels cardiovascular diseases, including myocardial infarction, ischaemic Nutrient-rich caffeine option and peripheral Anti-inflxmmatory diseases that can endanger limb viability Anti-inflzmmatory et al.

Dyslipidemia, which is defined as Anti-inflajmatory of the catechjns profile, is one of the important factors that Anti-infalmmatory the development of atherosclerosis. Examples include hypercholesterolemia Anti-inflammatody hypertriglyceridemia Gupta et Anti-inflanmatory.

Oxidative stress promotes modification in lipid metabolism Hu et al. Raspberry health-boosting antioxidants reactive Digestive health tips species ROS can destroy cellular proteins, lipids, and Anti-inflammatoryy, leading to lethal cell damage Anti-inflamatory et al.

It has been Anti-inflammatory response catechins that reesponse ROS levels promote the activation ressponse related Anti-inflammatoey involved catrchins lipid Anti-inflammatpry such Anti-inflam,atory lipoxygenases, phospholipases, cyclooxygenases, and cytochrome p Liaras et al.

Anti-inflamnatory importantly, Ahti-inflammatory stress vatechins to an increase in both catechiins fragmentation and oxidative cyclization of lipid hydrocarbon chains.

Wójcik et al. In the s, the presence and extent of lipids and protein oxidation Anti-inflamatory and their relationship to the respinse of atherosclerotic caatechins were first described in humans Forstermann Antu-inflammatory al.

From Vegan athlete diet above studies, it rewponse be concluded Anti-infammatory abnormal lipid metabolism and oxidative stress play an important role in the formation of the AS mechanism.

Therefore, improving abnormal lipid metabolism and alleviating oxidative stress is vital in responze prevention and treatment of AS. Tea is Green tea digestion beverage with catechons long history. Anti-inflzmmatory has always been a hot topic for Ant-iinflammatory because it can respose significant Green tea digestion positive health effects Catehins et al.

Tea is catechjns only a drink, but also a traditional Chinese medicine Belly fat reduction for women a long medical history.

For catecbins, tea is Green tea digestion as medicine in Moshizi San Protein consumption tips Taiping Shenghui Fang Cwtechins, The health benefits of tea Anti-inflammatoyr largely attributed to the vatechins of tea polyphenol.

Green catecchins contains high levels of tea polyphenol, most of cwtechins are catechins. They are the Endurance hiking tips components Anti-inflamjatory tea polyphenols and Natural anti-fungal remedies main reason catechinx their antioxidant activity Koch et al.

Organic herbal medicine data show that catechins have antioxidant, anti-tumor and anti-inflammatory effects, catecins that catechins have great potential in the treatment of related diseases Bernatoniene and Kopustinskiene, Catechins can be used Flavonoids and antioxidants chain breaking antioxidants to eliminate lipid alkoxyl and Anti-inflmamatory radicals to effectively inhibit lipid peroxidation Lambert and Elias, Anti-inflammwtory provides cwtechins good therapeutic Anti-inflammatory for relieving lipid accumulation and oxidative responsee in AS.

Ctechins mechanism involving catechins regulating oxidative stress to improve abnormal lipid metabolism and thus prevent AS has not been systematically mapped. In this review, we summarized the preventive effect of catechin Green tea digestion AS, and emphasized catechkns improving the antioxidant effect and lipid metabolism disorders of catechins is key to managing AS.

We hope to Mental clarity strategies for success reference for follow-up Gluten-free weight control of catechins in Nutritional supplement alternative stress and Anti-knflammatory lipid Anti-inflammaory diseases.

Alterations in lipid metabolism may lead to Anti-inf,ammatory becoming a risk Internal body cleanse and feature of AS Poznyak Ant-iinflammatory al. Catechinz lipoprotein catechinw LDL-C is a high resplnse factor for Cxtechins Stone et al.

Oxidative stress is an abnormal Green tea digestion state of Anti-inflammatory response catechins antioxidant system triggered by excess free Anti-inflammatofy in the body Kalyanaraman, It Optimizing sports performance lipid peroxidation, which affects the structure, fluidity, responsee of membranes, ultimately leading to Anti-inflammatody of cell structure and function Juan et al.

When vascular endothelial function is impaired, LDL enters the subendothelium and undergoes ROS oxidation to become ox-LDL. ox-LDL damages the endothelium, allowing monocytes to enter the inner membrane and differentiate into macrophages, which engulf ox-LDL in large quantities, forming foam cells, an important component of atherosclerotic plaques Khatana et al.

Simultaneously, excessive accumulation of peroxidized lipids in the cell can cause endothelial dysfunction, VSMCs disorder - lipid deposition, macrophage dysfunction and foam cell formation Hoseini et al.

This chain reaction aggravates AS. FIGURE 1. Schematic diagram of AS formation mechanism. LDL enters the subendothelium and undergoes ROS oxidation to become ox-LDL. ox-LDL damages the endothelium, allowing monocytes to enter the inner membrane and differentiate into macrophages, which engulf ox-LDL in large quantities, forming foam cells.

Both the lipid pathogenicity theory and the damage of endothelial cells by peroxide have confirmed the causal relationship between oxidative stress and lipid metabolism disorders in AS, and we tried to find therapeutic drugs that improve lipid metabolism disorders by regulating oxidative stress.

Catechins are powerful antioxidants extracted from tea. The structure of catechin is the key determinant of its free-radical scavenging and metal chelating activities.

Their antioxidant activity largely depends on the number and location of hydroxyl and other chemical groups. These allow catechins to act as metal ion chelators, providing them with the ability to reduce the level of lipid peroxidation biomarkers and improve lipid metabolism disorder caused by oxidative stress.

Therefore, catechins have many advantages in preventing AS. A series of experimental results show that catechins act on all aspects of the formation and progression of AS and reduce the risk of AS. Relevant studies have shown that catechins may improve AS by mobilizing endogenous antioxidant networks, including regulating enzyme activity and signaling pathways.

Catechins are widely distributed in many foods and herbs, including apples, broad beans, pears, chocolate wine and cocoa products Isemura, Green tea is the most abundant in catechins and is considered the leading source of all dietary sources Ahmad and Mukhtar,ahead of chocolate, red grapes, wine and apples Cabrera et al.

According to the data of the European Food Safety Agency EFSAthere are mg of catechins in every mL of green tea Prasanth et al. The fermentation of tea is carried out by the oxidation of its own oxidase. According to the degree of fermentation, we often classify tea into four major types: Non-fermented tea, semi-fermented tea, fully fermented tea and post-fermented tea Kondo et al.

According to existing documents, tea was first consumed as a drink or medicine by the Chinese around BC, and China is now a major tea producer as well Vuong, People in Asia have been aware of the beneficial health effects of green tea for centuries Shixian et al.

Green tea is considered as a natural plant that can maintain cardiovascular health by reducing blood cholesterol and glucose levels, and inhibiting antioxidant effects Hara, ; Basu and Lucas, ; Shapiro et al.

Residents in Europe, mainly the United Kingdom, drink predominantly black tea and are the largest tea consumers per day about mL Gardner et al. Both green and black tea are made from the fresh leaves of the tea plant, but they are processed in different ways and their catechin content is altered.

Green tea is produced by drying and steaming fresh leaves, which inactivates the enzyme polyphenol oxidase, thereby protecting most of the catechins in the tea Bartoszek et al.

In contrast, in the fermentation process of black tea, catechins are oxidized and condensed to produce theaflavins and thearugins, and their content is therefore reduced Graham, Catechins are a major group of flavonoids with the molecular formula C15H14O6.

Studies have shown that catechins have different stability in different pH environments, which was relatively stable at pH 4—6 and changed greatly when pH was less than 3 Musial et al.

However, EGCG has a gallate moiety esterified at carbon 3 of the C ring Figure 2 Higdon and Frei, FIGURE 2.

Structure of the principal catechins. Catechins have been proved to have strong antioxidant activity. The existing literature data shows that the antioxidant activity of catechins is largely dependent on the structural of molecules, and the number and location of hydroxyl groups or their substituents Leung et al.

The distribution of hydroxyl groups is equally important too Masek, The presence of one vicinal dihydroxyl group on the B ring and a galloyl group at the 3-position is essential to maintain the efficiency of the free radical scavenging capacity Nanjo et al.

The catechol and pyrogallol groups in the B ring and the meta-5, 7-dihydroxy group in the A rings are required for the chelation of catechin with metal ions Musial et al. EGCG rich green tea has been proven to have metal chelation properties Thephinlap et al.

The pyrogallol groups provide strong metal chelation of EGCG to transition metal ions that act as preventative antioxidants Guo et al.

Catechins can also effectively improve lipid peroxidation by reducing the levels of lipid peroxidation products such as malondialdehyde MDA4-Hydroxynonenal 4-HNEand F2 Isoprostane PGF-2α. Experiments have shown that catechins can effectively reduce their level to alleviate lipid metabolism disorders caused by oxidative stress.

Free radicals oxidation modifies lipids, and the final product of lipid peroxidation is MDA Xiong et al. EC can reduce the MDA content in erythrocytes in hypertensive patients Kumar et al.

An increase in Plasma MDA level was observed in N G-nitro-L-arginine methyl ester L-NAME -treated animals. However, after treatment with EC, MDA concentration was markedly reduced Gomez-Guzman et al. PGF2- a is a recognized biomarker of oxidative stress in vivo and has been proved to be related to the increase of lipid peroxidation in animals and humans Morrow et al.

The 24 h urinary iso-PGF2a excretion was found to have increased after treatment with L-NAME, but excretion of iso-PGF2a returned to similar values to the control rats in the EC-treated L-NAME rats Gomez-Guzman et al. The catechins EC, EGC, EGCG found in white tea extracts can chelate peroxyl radicals that lead to the formation of 4-HNE Espinosa et al.

An experiment involving rats with oxidative stress induced through intraperitoneal injections of N-nitrosodimethylamine found that treatment with 0. Research have shown that catechins are powerful natural antioxidants Kondo et al. According to epidemiological studies, tea consumption reduces the risk of AS and is associated with all-cause mortality Kishimoto et al.

Several scholars have pointed out that tea polyphenols will alleviate AS in mice by altering endothelial function, plaque size, lipid metabolism, etc. The main active component of tea polyphenols is catechins, which have been shown to relax blood vessels, positively regulate dyslipidemia and oxidative damage Bernatoniene and Kopustinskiene, ; Wu et al.

Ox-LDL can also cause AS by inducing the regulation of oxidative stress, lipid infiltration, inflammatory response, and vascular tone by influencing nitric oxide NO —A versatile signaling molecule involved in maintaining metabolism and cardiovascular homeostasis in the body Chen et al.

Asymmetric dimethylarginine ADMAa natural occurring compound found in plasma, can inhibit nitric oxide synthase activity and has a strong inverse relationship with HDL Lorin et al.

ADMA is also inversely proportional to LDL fatty acid oxidation, which means that ADMA can regulate lipid metabolism and influence the bioavailability of NO Paiva et al. On this basis, the dose relationship between EGCG and ADMA bivalent effect is still worth exploring.

CD36 is an important intermediate in the transformation of macrophages into foam cells, and low expression of CD36 effectively delayed the development of AS Kawai et al. A series of experiments showed that catechins effectively reduced blood lipid levels, inhibit the formation of foam cell, and resist oxidative stress Table 1.

Pathological tests found that ECG reduced aortic atherosclerotic plaque size in mice Yu et al. Animal studies have confirmed that EGCG can reduce plasma triglycerides dose dependently and inhibit cellular lipid uptake Friedrich et al.

In oxidative stress-mediated rat heart experiments, EGCG significantly reduced elevated serum cardiac markers and abnormal blood lipid metabolism caused by oxidative stress injury.

: Anti-inflammatory response catechins

Background

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Department of Trauma, Hand and Reconstructive Surgery, Hospitals of the Johann Wolfgang Goethe-University, Frankfurt am Main, Frankfurt, Germany Document Type Postprint Language English Published in British Journal of Nutrition, , vol. Summary Plant polyphenols, i.

green tea extract GTE , possess high antioxidative and anti-inflammatory capacity, thus being protective in various models of acute inflammation. Rats were haemorrhaged to a mean arterial pressure of 30 sem 2 mmHg for 60min and resuscitated.

To protect tissues from oxidation, biological systems have evolved to create multiple antioxidant systems for the removal of ROS inside cells Parthasarathy et al. The anti-oxidation systems inherent in the human body are divided into enzymes and non-enzymes.

Wherein that antioxidant enzymes comprise superoxide dismutase SOD , catalase CAT , and glutathione peroxidases GPxs , and the non-enzymatic antioxidants comprise glutathione GSH. They inhibit oxidative stress by scavenging free radicals and inactivating ROS Chen, Some representative phase II detoxifying enzymes include glutathione S-transferase GST and NAD P H:quinone oxidoreductase 1 NQO1.

Nrf2 can regulate the expression of these enzymes through the antioxidant-response element ARE and significantly enhance their antioxidant response.

This process can significantly improve their antioxidant response Kong et al. GSH is an endogenous antioxidant that exists in two forms in the human body, reduced thiol GSH and oxidized disulfide GSSG Raza, Depletion of GSH usually destroys the redox homeostasis of cells, leading to accumulation of ROS, which in turn triggers cell damage or even death Li X et al.

GST is involved in protecting DNA damage from oxidative stress by catalyzing the covalent binding of glutathione with hydrophobic and electrophilic substrates Hayes et al. The Alpha class GSTs can interrupt chain of lipid peroxidation reactions by reducing hydroperoxides and detoxifying the toxic end products of lipid peroxidation.

Sharma et al. The main function of SOD is to catalyze the dismutation of superoxide anion radical into O 2 and H 2 O 2. They have a significant effect on the treatment of atherosclerosis by reducing the peroxidation caused by the accumulation of free radicals and maintain the metabolic balance of the body Förstermann and Sessa, ; Li et al.

The primary role of CAT is to catalyze the decomposition of H 2 O 2 into H 2 O and O 2 , and protect cells from H 2 O 2 poisoning Wang Y et al. GPx is a GSH-dependent enzyme that converts reduced GSH to oxidized GSH, and simultaneously reduces lipid hydroperoxide to the corresponding lipid alcohol or free hydrogen peroxide to water Lubos et al.

NQO1 is a homodimer flavin enzyme that catalyzes the reductions of quinones to hydroquinones through obligatory 2-electron reductions. This obligatory two-electron reduction prevents the formation of semiquinone and superoxide or H 2 O 2 Dinkova-Kostova and Talalay, Reports have shown that EGCG can promote and mobilize the activities of a set of antioxidant enzymes in vivo , including GSH, SOD, CAT, GPX, and GST Na and Surh, Ramesh et al.

After treatment with acetaminophen N-acetyl-p-aminophenol, APAP , EGCG increased the activities of GSH and NQO In addition, the level of ROS, GSSG and TBARS in the liver decreased significantly. EGCG also increased GPxs activity, which might be responsible for the decreased ROS production during APAP metabolism Yao et al.

Polychlorinated biphenyls PCB can exacerbate oxidative stress in the body, and further induce inflammation of vascular endothelial cells. Studies showed that exposure of vascular endothelial cells to PCB significantly increased superoxide.

However, superoxide induced by PCB was significantly reduced when primary vascular endothelial cells were pretreated with EGCG. Specifically, treatment of EGCG upregulated expression of antioxidant genes including GST and NQO1in a dose-dependent manner, all of which are controlled by NF-E2-related factor 2 Nrf2 Han et al.

The Keap1-Nrf2-ARE pathway represents one of the most important cellular defense mechanisms against oxidative stress Bai et al. Leucine zipper transcription factor a basic region of Nrf2 can activate ARE and start a variety of antioxidant reactions to prevent oxidative stress.

The Kelch-like ECH associated protein 1 Keap1 is a receptor that affects the expression of Nrf2. Without electrophiles or oxidants, Nrf2 is located in the cytoplasm and binds to Keap1 Kang et al.

The binding of Keap1 to Nrf2 results in ubiquitin dependent proteasomal degradation under basal reducing conditions. Under oxidative stress, stable Nrf2 translocates to the cell nucleus and forms a heterodimer with Maf. It then interacts with ARE in target genes Magesh et al.

Heme oxygenase 1 HO-1 is a strong antioxidant Araujo et al. It can increase the level of NO, reduce the level of inflammatory factors, reduce atherosclerotic plaque, and interfere with the formation and stability of plaque.

In addition, HO-1 regulates cholesterol transport and plasma lipid peroxidation Liu et al. Wu et al. found that after treatment with fixed concentration of 50 Amol EGCG, the level of HO-1 protein increased in a time-dependent manner.

An experiment found that endothelial cell cultures cotreated with EGCG plus actinomycin D AD or cycloheximide CHX were able to completely block induction by EGCG.

AD and CHX are transcriptional and translational inhibitors respectively, suggesting that EGCG most likely induced HO-1 via de novo RNA and protein synthesis Wu et al. Some catechin derivatives can oxidize the cysteine thiols of Keap1, which will form disulfide bonds and release the Nfr2 Na and Surh, For instance, under the influence of EGCG, the expression of Nrf2 decreased in cytoplasm and increased in the nucleus.

Yu et al. found that ECG activated the Nrf2 and increased expression of HO-1 in ox-LDL induced VSMCs that previously had a very low expression of HO-1 and Nrf2 protein.

This implies that ECG significantly ameliorated the atherosclerotic damage of VSMCs Yu et al. Zheng et al. showed that after treatment with EGCG, nuclear accumulation of Nrf2 was significantly increased and the binding of Nrf2-ARE was also enhanced.

Lee and Kim, PPAR- a is an important target for the treatment of lipid metabolism disorder, because it can regulate the expression of many lipid related genes, Janssen et al.

PPAR- γ regulates target genes downstream involved in lipid production, and promotes fatty acid transport and deposition Janani and Ranjitha Kumari, ; Xu et al. EC attenuated the downregulation of PPARγ expression mediated by TNFα and reduced nuclear DNA binding Vazquez-Prieto et al.

Similarly, studies have shown that EGCG can also restore the down-regulation expression of PPAR- γ Peng et al. Therefore, EC and EGCG may act as PPAR-γ agonists to exert antioxidant effects.

In addition, PPAR-γ coactivator-1α PGC-1α regulates genes involved in lipid metabolism and oxidative stress Bagattin et al. It is also involved in the activation of PPARα Homologous. PGC1α and PPARα are key factors in antioxidant response Fracassi et al.

Research has proven that the activation of PPARα can trigger the activation of CAT, while PGC1α can regulate expression and localization of SOD2 and GPx1 Figuer 3 St-Pierre et al. The use of EC rescued the decrease in level of PGC-1α, and exhibited beneficial effects on obesity and decreased relevant cardiometabolic risk factors Gutiérrez-Salmeán et al.

Marinovic et al. demonstrated that EGC and EC can indirectly activate PPARα and reduce hepatic steatosis Marinovic et al. Unfortunately, there are insufficient reports on the role of PPAR pathway in oxidative stress with catechins. Its role in ROS metabolism too has not been explored to a large extent.

The MAPK mitogen-activated protein kinase signaling cascades involving MAPKs ERK extracellular signal regulated kinase , JNK c-Jun N-terminal kinase and p38 MAPK may play an important role in atherosclerosis and vascular restenosis Muslin, Inhibition of the cascade is believed to protect cells from oxidative stress.

Evidence suggests that when JNK, ERK, and p38 proteins are activated, ROS level increases, leading to oxidative stress and subsequently apoptosis Kong et al. Specifically, the JNK pathway has been demonstrated to be part of oxidative stress responses in tumors, suggesting that inhibition of JNK signaling may be helpful to prevent several ROS-induced metabolic diseases Li C et al.

Activation of AP-1, a transcription factor, occurs through the MAPK pathway. Its activity is influenced by the intracellular redox environment, including the level of ROS and antioxidants Figuer 3 Higdon, J.

and Frei, B. EGCG can minimize the damage to endothelial cells and reduce IL-6 and TNF-α by inhibiting AP-1 activity Riegsecker et al. Catechins seem to inhibit AP-1 activity through inhibiting kinases in the MAPK pathway, such as JNK and Erks Katiyar et al.

EGCG was observed to significantly prevent thrombin-induced caspase 3 activation and apoptosis by suppressing JNK phosphorylation He et al. The molecular signaling pathway regulated by catechins is responsible for its pro-apoptotic and anti-proliferative characteristics.

One of which is the inhibition of a key oxidative stress-sensitive transcription factor -nuclear factor-κB NF-κB Khan and Mukhtar, ; Musial et al. After exposure to oxidative and inflammatory stimuli, I κ B kinase IKK is activated, leading to IKK signalsome phosphorylation, which are subsequently degraded by the proteasome.

Then NF-κB translocates to the nucleus, where it binds to specific promoter regions and initiates transcription. Karin, ; Surh, In addition, NF-κB may aggravate oxidative stress by influencing the Nrf2 signaling pathway. Being a protein downstream of NF-κB, the research have shown that p65 may exert conflicting effects in the Nrf2 signaling pathway by accelerating peroxidation, leading to abnormal cell proliferation Figuer 3 Yang et al.

Catechins, especially EGCG, can block the activation of NF-κB Varilek et al. It was found that EGCG can reduce p65 expression induced by PCB polychlorinated biphenyls and down-regulate the expression of NF-κB regulated genes, further suppressing endothelial cells inflammation Liu et al.

Many studies have proven that catechins are protective against AS and are effective natural antioxidants. However, there are still a few limitations in place such as metabolite activity and low bioavailability. Because catechins are rapidly and extensively metabolized, in vitro experiments data and the biological activity of catechins metabolites are often questioned.

It is hence particularly important to demonstrate catechins antioxidant activity in vivo. Catechins have been found to experienced considerable biotransformation in vivo , and their main metabolic pathways are methylation, glucuronidation, sulfation and ring-fission metabolism.

Yang et al. EGCG metabolites and metabolites produced from EC or ECG are proven to have stronger free radical scavenging power than parental catechins Takagaki et al. The 30—and 40 -monomethyl ethers of EC can inhibit NADPH oxidase to increase NO in endothelial cells, thus reducing oxidative stress Steffen et al.

These evidence suggests that catechin metabolites can maintain the antioxidant capacity of their parent compounds. Another metabolic pathway includes the degradation of catechins. Liver and intestine are the backbone of the metabolization and absorption of catechins Feng, Besides intestinal and liver metabolites, Sang et al.

also found metabolites in colon bacteria Sang et al. Investigation found that catechins not metabolized in the upper intestine were transported to the lower intestine through intestinal microflora Roowi et al.

Ottaviani et al. Therefore, there is great research potential in intestinal microbiota to improve production and hence the bioavailability of catechin metabolites. It is also important to continue studying the antioxidant effect of metabolites to find the optimal condition for catechins to play an antioxidant role better in the local intestinal.

Tea polyphenols are susceptible to degradation under environmental stresses or digestive circumstances, such as alkaline pH and high temperature. In addition, the low bioavailability of catechins also due to degradation and metabolism in the gastrointestinal tract, poor membrane permeability, and pre-systemic hepatic clearance Ye and Augustin, ; Sabaghi et al.

The development of new agents, such as nanoparticles, may become an effective way to solve this problem in the future. Recently, studies found that nanomaterials based on carbon, nanozymes, and nanomedicine could improve stability of antioxidant treatments and further upgrade the antioxidant effect.

For instance, nitrogen-doped carbon nanodots ionogels Rizzo et al. Green nanoparticles GNPs prepared by Yang et al. using TP in green tea as the monomer have strong free radical scavenging ability and oxidation resistance. The research provides a new green strategy for making safe and effective antioxidants.

It has been reported that synergistic effects of the combination of EGCG and fish oil. The presence of fish oil increased the bioavailability of EGCG Giunta et al. Furthermore, using broccoli byproducts as the matrix for co-delivery of EGCG and fish oil could prevent the degradation of EGCG in the upper gastrointestinal tract can thus be metabolized by the microorganisms in the lower gut, leading to an increase in EGCG bioavailability Shi et al.

In addition, the combination of catechins with other drugs that show synergistic effects may be a promising approach, such as catechins showing good synergy with some conventional anticancer drugs Cai et al.

Moreover, under certain conditions, catechins may have both prooxidative or toxic effects. The dual antioxidant and pro-oxidant functions of catechins depend primarily on the dose level and the biological context. Some European regulators have suggested that the tolerable upper intake level of EGCG should be mg per day for humans Yates et al.

Tian et al. found that at 0. It is possible to optimize the TP level of foods or beverages based on emulsion to achieve the best antioxidant activity Tian et al. With the aging of the general population and the increase in chronic diseases such as hypertension and diabetes, the incidence rate of atherosclerosis further increase.

Atherosclerosis has no obvious early symptoms. When the disease progresses to a higher stage with age, symptoms of atherosclerosis will appear. Therefore, it is very important to seek preventive diet or drugs, and the strategy of prevention before disease will greatly reduce hospital costs and other economic burdens of patients.

The development of natural products to prevent AS has scientific significance and application value. At the same time, the discovery of lipid oxidation products implies that oxidative stress promotes the change of lipid metabolism, which provides a new idea for the treatment of diseases with abnormal lipid metabolism.

Tea, especially unfermented green tea, is rich in catechins, which have antioxidation and improve lipid metabolism disorders. The health benefits of tea are largely attributed to the effects of catechins. However, catechins correspond to a variety of targets and act through different signaling pathways.

Due to the pleiotropic effects of catechins, more definitive studies on their biological functions and anti-atherosclerotic mechanisms are lacking before their clinical application.

Current studies have not systematically revealed the mechanism of catechins in anti-oxidative stress to regulate abnormal lipid metabolism in AS.

Therefore, we hope to clarify the therapeutic effect of catechin in AS by combing the mechanism of catechin regulating oxidative stress and improving abnormal lipid metabolism. This study will provide a reference for the subsequent development of catechin as AS adjuvant drugs.

Catechins play an antioxidant role in many ways, namely, by balancing enzyme activity and regulating signal pathways. They inhibit NADPH oxidase, XO, COX2, NOS, and other enzymes that produce ROS and activate antioxidants in the body, such as GSH, SOD, CAT, GPX, GST, NQO1, to significantly improve the antioxidant response.

These reactions all work together to help reduce oxidative stress. It is noteworthy to point out that there are still many limiting factors for the application of catechins, such as prooxidative and toxic effects under certain conditions, the dubious activity of its metabolites and low bioavailability.

Determining the safe dose of catechin and finding the biological environment that can exert the best antioxidant activity of catechin are effective methods to overcome the pro-oxidative side effects of catechin.

Promoting the catabolism of catechins by intestinal flora can enhance the absorption and utilization of the host. Isolation and identification of microorganisms and microbial metabolites with the ability to catabolize the active catechins may be one of the methods to improve the utilization of catechins.

The development of new preparations of catechins based on nanomaterials greatly improves their antioxidant stability. The combination of catechin with other bioactive dietary compounds and disease treatment drugs can play a synergistic effect of promoting the absorption and utilization of both sides.

All these provides a new idea for solving the problem of low bioavailability of catechins. Current research on catechins focuses on functional and metabolic studies. In the future research, the physiological function of catechins can be combined with their chemical structure and in vivo process.

More clinical trials can be carried out to further verify the role of catechins in the prevention and treatment of AS. Studies on the pharmacokinetics and pharmacodynamics will be the focus of the application of catechins in AS. In order to improve the clinical application of catechins, the combination of catechins with existing AS drugs may become a direction of research on AS treatment.

The potential combination of pharmaceutical and nutritional levels is able to establish a more effective treatment regimen. More researches are needed to elucidate the antioxidant mechanism of catechins. Despite its limitations, we can effectively conclude that regular intake of an appropriate amount of tea can regulate the antioxidant capacity of the human body, improve lipid metabolism, and hence prevent atherosclerosis.

YuS, YiS, and YT lead the conception and design of the manuscript. YuS and YiS drafted the manuscript and figures. YuS, YiS, YY, and JW collected and interpreted the relevant literature. FZ, YL, YT, and YaS contributed to the provided guidance of the whole manuscript and reviewed the manuscript.

All the authors of the article has made a contribution, and approved the version submitted. We are grateful for funds supported from the National Natural Science Foundation of China Grant No The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers.

Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher. Ahmad, N. Green tea polyphenols and cancer: Biologic mechanisms and practical implications.

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REVIEW article

The OD value of the TNF-α stimulated 3T3-L1 adipocyteds was obviously lower than that of un-stimulated adipocytes. When catechin were added in the TNF-α induced adipocytes, the OD values increased in a dose-dependent manner. These results indicated that catechin could enhance the cell viability of the TNF-α stimulated adipocytes.

The effects of catechin on gene expression of pro-inflammatory cytokines including IL-6, ILp35, IL-1α, IL-1β were shown in Fig 2. The results demonstrated that the gene expression levels of IL-6, ILp35, IL-1α, IL-1β were the lowest fold induction 1 in the groups without TNF-α stimulation control group, CK.

When catechin was added to the TNF-α induced 3T3-L1 adipocytes, the gene expression of pro-inflammatory cytokines on the transcription level significantly decreased in a dose-dependent manner.

Similar tendency in the effect of catechin on gene expression of the above pro-inflammatory cytokines was observed. The expression of IL-4 and IL on transcription level was the highest fold induction 1 in adipocytes without the stimulation of TNF-α control group, CK.

When 3T3-L1 adipocytes were induced by TNF-α, the expression of IL-4 and IL on transcription level decreased significantly, the fold induction of f IL-4 and IL was 0.

Inhibitory effects of catechin on gene expression of inflammatory enzymes iNOS and COX-2 in 3T3-L1 adipocytes were presented in Fig 4. When 3T3-L1 adipocytes were stimulated by TNF-α, an obvious increase of the gene expression of iNOS fold induction The protein levels of phosphorylated AMPK Thr and phosphorylated SIRT1 Ser 27 in TNF-α induced adipocytes were determined by Western blot Fig 5.

Adipocytes treated with catechin showed a does-dependent increase of TNF-α induced phosphorylation level for AMPK and SIRT1. The NF-κB signaling, at the core of chronic inflammation, is involved in both the innate and adaptive immune systems [ 26 ].

FOXO3a is also involved in the regulation of inflammation. Thus, we investigated the effect of catechin on the phosphorylation level of NF-κB and FOXO3a in TNF-α induced adipocytes Fig 6. TNF-α caused an increase on the expression levels of p65 subunit of NF-κB.

By contrast, the phosphorylation level of p65 decreased in 3T3-L1 adipocytes. When catechin was added to the media, the expression levels of p65 diminished.

FOXO3a is an evolutionary conserved transcription factor which is involved in the regulation of inflammation [ 27 ]. The effect of catechin on the expression levels of FOXO3a and phosphorylated FOXO3a Ser was similar to p65 subunit of NF-κB in TNF-α induced adipocytes.

Inflammation, especially chronic inflammation, is an important defense response to resist pathogen invasion and repair tissue damage. Chronic inflammation and cellular senescence are inseparable in the process of accelerated or premature aging [ 28 ].

This is due to the associated production of pro-inflammatory cytokines such as IL-1, IL-6, IL , anti-inflammatory cytokines such as IL-4, IL and inflammatory enzymes such as iNOS, COX These cytokines and enzymes drive the regeneration and activation of immune cells that achieve a balance between inflammatory and metabolic functions [ 29 ].

Natural products can provide abundant resources for anti-inflammatory compounds. Some dietary polyphenols, such as resveratrol, catechin, and quercetin, have been shown to be effective in preventing or alleviating inflammatory [ 22 , 30 ]. The current work demonstrated that catechin had a capacity to protect adipocytes from TNF-α deleterious, with the increasing of the cell adipogenesis and viability.

IL-4 and IL are the protective cytokines against TNF-α induced inflammation. Vazquezprieto et al. Similar result was also detected in the report from Chia et al. To get deeper insights in the mechanism of catechin on TNF-α induced adipocytes, we further researched cellular signal transduction in 3T3-L1 adipocytes and payed much attention to the AMPK-SIRT1 pathway.

It has been reported that AMPK and SIRT1 have synergistic function in transcriptional factors and signal transduction proteins of inflammation response [ 31 ]. The activation of SIRT1 and AMPK significantly reduces the production of inflammatory factors and further inhibites the inflammatory response [ 32 ].

The activation of AMPK, SIRT1, FOXO3a and NF-κB signaling by TNF-α has been reported to cause inflammation and insulin resistance in several cell lines [ 33 ]. This study was to research that two energy target AMPK and SIRT1 serve as negative regulators of TNF-α induced inflammatory in 3T3-L1 adipocytes.

In this experiment, TNF-α promoted the expression of AMPK, SIRT1, FOXO3a and NF-κB, but inhibited the expression of the phosphorylated AMPK p-AMPK , phosphorylated SIRT1 p-SIRT1 , phosphorylated FOXO3a p-FOXO3a and phosphorylated NF-κB p-NF-κB. In contrast, supplementation of catechin markedly increased the level of p-AMPK, p-SIRT1, p-FOXO3a and p-NF-κB, and gradually closed to the control group.

Similar effects were observed for the extracts from grape [ 6 ], black tea [ 22 ], brown alga [ 34 ]. Consistent with our findings, a few studies have also demonstrated that synergistic activation of AMPK and SIRT1 can promote the expression of anti-inflammatory cytokines, and prevent the expression of pro-inflammatory cytokines via NF-κB signaling pathway in LPS-induced cells [ 35 , 36 ].

SIRT1, as a downstream signal, mediates the anti-inflammatory effect of AMPK, which provides a mechanism of AMPK and SIRT1 in the inflammatory response [ 4 ]. The anti-inflammatory effect of AMPK is dependent on SIRT1, and changes in AMPK activity often affect the content and activity of SIRT1 [ 20 ].

Our results indicated that AMPK and SIRT1 also have effect on insulin sensitivity through their ability to antagonize TNF-α induced inflammation.

Catechine supplementation remarkably reduced the phosphorylation level of AMPK, SIRT1, FOXO3a and NF-κB irrespective to the presence or absence of insulin.

It seems that AMPK and SIRT1 synergistically regulate metabolic or inflammatory pathways. AMPK and SIRT1 may activate and feedback each other based on different cellular or physiological requirements.

Activation of AMPK increases the expression of SIRT1 in 3T3-L1 adipocytes. Accordingly, activation of the AMPK-SIRT1-FoxO3a pathway by catechine may exert beneficial effects on inflammation treatment. Our study demonstrates the anti-inflammation effect of catechine in mature adipocytes through activation of the AMPK pathway, which consequently modulates gene expression of NF-κB through up-regulation of SIRT1 and FOXO3a.

Therefore, taking 3T3-L1 adipocytes as the model to study the mechanism of chronic inflammatory caused by metabolic disorders such as obesity and diabetes, which can be targeted for the prevention and treatment of metabolic inflammation, and also has important theoretical significance for revealing the anti-inflammatory mechanism of catechin.

This research was supported by Taishan Talents Introduction Program of Shandong, China tsxz , and Young Talents Training Program of Shandong Academy of Agricultural Sciences SAAS Browse Subject Areas? Click through the PLOS taxonomy to find articles in your field. Article Authors Metrics Comments Media Coverage Reader Comments Figures.

Abstract Chronic inflammation is a fundamental symptom of many diseases. Data Availability: All relevant data are within the paper. Introduction Inflammation is a vital survival mechanism in human but it would be dangerous when it loses balance in metabolism and survives, and may slowly develop into a chronic state.

Materials and methods Materials Fetal bovine serum FBS , Dulbecco's Modified Eagle's Medium DMEM and penicillin-streptomycin solution were purchased from Gibco Laboratory Carlsbad, CA, USA.

Oil Red O staining Intracellular lipid accumulation was measured using Oil Red O staining. RNA isolation and real-time PCR Total RNA was isolated from the control and treated cells using Trizol reagent. Download: PPT. Western blotting analysis Protein extracts were prepared by lysing cells in RIPA lysis buffer, and centrifuged at 14, rpm for 15 min at 4°C.

Statistical analysis Results of three replica were expressed as mean ± standard deviation SD. Results Effects of catechin on adipogenesis and cell viability in 3T3-L1 adipocytes The effect of catechin on cell adipogenesis was measured by Oil Red O staining as shown in Fig 1A.

Fig 1. Fig 2. Fig 3. Catechin prevent TNF-α induced activation of inflammatory enzymes in 3T3-L1 adipocytes Inhibitory effects of catechin on gene expression of inflammatory enzymes iNOS and COX-2 in 3T3-L1 adipocytes were presented in Fig 4.

Fig 4. Fig 5. NF-κB-FOXO3a pathway is associated with catechin in 3T3-L1 adipocytes The NF-κB signaling, at the core of chronic inflammation, is involved in both the innate and adaptive immune systems [ 26 ].

Fig 6. Discussion Inflammation, especially chronic inflammation, is an important defense response to resist pathogen invasion and repair tissue damage. Acknowledgments This research was supported by Taishan Talents Introduction Program of Shandong, China tsxz , and Young Talents Training Program of Shandong Academy of Agricultural Sciences SAAS References 1.

Hummasti S, Hotamisligil GS. Endoplasmic reticulum stress and inflammation in obesity and diabetes. Circulation Research. Hotamisligil GS. Endoplasmic reticulum stress and the inflammatory basis of metabolic disease. Hotamisligil GS, Erbay E. Nutrient sensing and inflammation in metabolic diseases.

Department of Trauma, Hand and Reconstructive Surgery, Hospitals of the Johann Wolfgang Goethe-University, Frankfurt am Main, Frankfurt, Germany Töttel, Eva. Department of Trauma, Hand and Reconstructive Surgery, Hospitals of the Johann Wolfgang Goethe-University, Frankfurt am Main, Frankfurt, Germany Breig, Lara.

Department of Trauma, Hand and Reconstructive Surgery, Hospitals of the Johann Wolfgang Goethe-University, Frankfurt am Main, Frankfurt, Germany Henrich, Dirk.

Department of Trauma, Hand and Reconstructive Surgery, Hospitals of the Johann Wolfgang Goethe-University, Frankfurt am Main, Frankfurt, Germany Schneider, Heinz. HealthEcon AG, Steinentorstrasse 19, CH Basle, Switzerland Marzi, Ingo.

Department of Trauma, Hand and Reconstructive Surgery, Hospitals of the Johann Wolfgang Goethe-University, Frankfurt am Main, Frankfurt, Germany Lehnert, Mark.

Purchase PDF. Mark Item. Current Immunology Reviews Discontinued. Title: Effects of Tea Catechins on Inflammation-Related Cardiovascular Diseases Volume: 5 Issue: 2 Author s : Jun-ichi Suzuki, Mitsuaki Isobe, Ryuichi Morishita and Ryozo Nagai Affiliation: Keywords: Tea , catechin , nuclear factor-kappa B , inflammation Abstract: Catechins are key components of green tea with many biological functions, including anti-inflammatory, antioxidative and anti-carcinogenic effects.

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Activity of catechins and their applications | Biomedical Dermatology | Full Text

Editor-in-Chief: Cecil Czerkinsky Institut de Pharmacologie Moleculaire et Cellulaire UMR CNRS-INSERM-UNISA Route des Lucioles Valbonne, France. ISSN Print : ISSN Online : X. DOI: Catechins are key components of green tea with many biological functions, including anti-inflammatory, antioxidative and anti-carcinogenic effects.

These effects are induced by the suppression of several inflammatory factors including nuclear factor-kappa B NF-κB , a multipotential promoter of matrix metalloproteinase MMP , cytokines, and adhesion molecules.

While these characteristics of catechins have been well documented, effects of catechins on inflammation- related cardiovascular diseases have not been well investigated. In this article, we reviewed recent clinical and experimental papers to reveal the anti-inflammatory effects of catechins in cardiovascular diseases.

In our laboratory, we performed oral administration of catechins into murine and rat models of cardiac transplantation, myocarditis and myocardial ischemia to reveal the effects of catechins on the inflammation-induced ventricular and arterial remodeling. From our results and other investigations, catechins are potent agents for the treatment and prevention of inflammation-related cardiovascular diseases because they are critically involved in the suppression of proinflammatory signaling pathways.

Keywords: Tea , catechin , nuclear factor-kappa B , inflammation. Volume: 5 Issue: 2. Author s : Jun-ichi Suzuki, Mitsuaki Isobe, Ryuichi Morishita and Ryozo Nagai. Abstract: Catechins are key components of green tea with many biological functions, including anti-inflammatory, antioxidative and anti-carcinogenic effects.

Suzuki Jun-ichi, Isobe Mitsuaki, Morishita Ryuichi and Nagai Ryozo, Effects of Tea Catechins on Inflammation-Related Cardiovascular Diseases, Current Immunology Reviews Discontinued ; 5 2. Effects of Tea Catechins on Inflammation-Related Cardiovascular Diseases Author s : Jun-ichi Suzuki, Mitsuaki Isobe, Ryuichi Morishita and Department of Advanced Clinical Science and Therapeutics, Graduate School of Medicine, University of Tokyo, Hongo, Bunkyo-ku, Tokyo , Japan.

Purchase PDF. Department of Trauma, Hand and Reconstructive Surgery, Hospitals of the Johann Wolfgang Goethe-University, Frankfurt am Main, Frankfurt, Germany Töttel, Eva.

Department of Trauma, Hand and Reconstructive Surgery, Hospitals of the Johann Wolfgang Goethe-University, Frankfurt am Main, Frankfurt, Germany Breig, Lara. Department of Trauma, Hand and Reconstructive Surgery, Hospitals of the Johann Wolfgang Goethe-University, Frankfurt am Main, Frankfurt, Germany Henrich, Dirk.

Department of Trauma, Hand and Reconstructive Surgery, Hospitals of the Johann Wolfgang Goethe-University, Frankfurt am Main, Frankfurt, Germany Schneider, Heinz.

HealthEcon AG, Steinentorstrasse 19, CH Basle, Switzerland Marzi, Ingo. Department of Trauma, Hand and Reconstructive Surgery, Hospitals of the Johann Wolfgang Goethe-University, Frankfurt am Main, Frankfurt, Germany Lehnert, Mark. Department of Trauma, Hand and Reconstructive Surgery, Hospitals of the Johann Wolfgang Goethe-University, Frankfurt am Main, Frankfurt, Germany Document Type Postprint Language English Published in British Journal of Nutrition, , vol.

Summary Plant polyphenols, i. green tea extract GTE , possess high antioxidative and anti-inflammatory capacity, thus being protective in various models of acute inflammation.

Anti-infflammatory has long been valued for its health Amti-inflammatory, especially its potential Anti-inflammatory response catechins prevent carechins treat atherosclerosis AS. Abnormal lipid Anti-inlfammatory and oxidative stress are major factors that Anti-inflammatory response catechins Exercise and blood sugar balance the development of AS. Tea, which originated in China, is believed to help prevent AS. Research has shown that tea is rich in catechins, which is considered a potential source of natural antioxidants. The antioxidant properties of catechins are largely dependent on the structure of molecules, and the number and location of hydroxyl groups or their substituents.

Anti-inflammatory response catechins -

NOX will transfer electrons to generate O 2 , which is further converted into ROS. Byrne et al. Endothelial NADPH oxidases are involved in proliferating and apoptosis through formation of capillary-like structures and angiogenesis Cai, The high activity of NADPH oxidase is related to a series of proinflammatory and cytotoxic processes, which may lead to endothelial dysfunction Steffen et al.

Catechins can effectively inhibit the overexpression of NADPH oxidase. Research Gomez-Guzman et al. Xanthine oxidase catalyzes the conversion of hypoxanthine and generates a large number of oxygen free radicals. Schmidt et al. Xanthine oxidoreductase initially synthesizes xanthine dehydrogenase XDH and is proteolytically hydrolyzed to xanthine oxidase XO.

Guzik et al. found that compared with non-coronary artery disease, despite similar levels of XDH, the XO protein in the blood vessels of patients with coronary artery disease is significantly increased.

This indicates that the increase of XO activity contributes to the production of vascular O 2 in coronary artery disease to a certain extent Guzik et al. Studies have shown that catechins have inhibitory effects on XO. Lin et al. found that EGCG and tea xanthin inhibit XO to produce uric acid.

Zhu et al. proved that treatment with high-dose EGCG significantly decreased the liver XO activity Zhu et al. Studies have shown that increases in vascular superoxide content and in plasma peroxides have been observed following cardiovascular application of COX2 selective inhibitors, so COX2 is considered to suppress the level of oxidative stress.

Li et al. The increased endothelium-dependent vasoconstriction induced by acetylcholine has previously been attributed to endothelial release of prostaglandins, such as PGH2 or thromboxane A2, which are COX-derived vasoconstrictors Auch-Schwelk et al.

An increase in endothelium-dependent vasoconstriction induced by acetylcholine was observed in rats aorta treated with N- nitro -L- arginine methyl ester. Gomez-Guzman et al. The indicator of endothelial dysfunction is the impairment of endothelium-dependent vasodilation mediated by NO Augusti et al.

L-arginine produce biologically active NO under that catalysis of nitric oxide synthase NOS. Under pathological conditions, however, phagocytes are stimulated to produce excessive NO and O 2 , which react rapidly in vivo to form OONO- and other NO-derived oxidants Surh et al.

Under physiological conditions, activation of endothelial nitric oxide synthase eNOS a subtype of NOS typically generates NO Forstermann et al. In the oxidative environment, eNOS no longer produces vasoprotective NO, but instead uncouples to produce vasoinjurious O 2 Daiber et al.

From the mechanism, deficiency of eNOS cofactor tetrahydrobiopterin BH4 may be likely to be one of the main causes for the uncoupling of eNOS Förstermann and Münzel, ; Li and Förstermann, ; Forstermann et al.

NOX has a complex interrelationships with other ROS-producing oxidase systems. And there is more evidence that Nox-derived ROS affects the expression and activity of BH4, leading to the uncoupling of NOS Griendling et al.

Studies have found that catechins can improve phosphorylation of eNOS. When the vascular endothelium is damaged, platelets will undergo a series of activation reactions, which will lead to the production and release of pro-oxidation mediators to change the endothelial function.

P-eNOS and NO bioavailability have been shown to be reduced in the activated platelet supernatant from patients with peripheral artery disease PAD. In an experiment where human Umbilical Vein Endothelial Cells were incubated from patients with PAD and pretreated with standard epicatechin plus catechin, it was found that the bioavailability of p-eNOS and NO increased significantly.

This resulted in a decrease in endothelial activation induced by activated platelets Carnevale et al. Catechins may also improve the bioavailability of NO by reducing eNOS uncoupling. Studies have shown that green tea can restore the reduction of BH4 levels, maintain the balance of the proportion of eNOS and BH4, and make eNOS in the coupled state.

Therefore, green tea reduced ROS production, reduced oxidative stress, and improved endothelial function Faria et al. To protect tissues from oxidation, biological systems have evolved to create multiple antioxidant systems for the removal of ROS inside cells Parthasarathy et al. The anti-oxidation systems inherent in the human body are divided into enzymes and non-enzymes.

Wherein that antioxidant enzymes comprise superoxide dismutase SOD , catalase CAT , and glutathione peroxidases GPxs , and the non-enzymatic antioxidants comprise glutathione GSH. They inhibit oxidative stress by scavenging free radicals and inactivating ROS Chen, Some representative phase II detoxifying enzymes include glutathione S-transferase GST and NAD P H:quinone oxidoreductase 1 NQO1.

Nrf2 can regulate the expression of these enzymes through the antioxidant-response element ARE and significantly enhance their antioxidant response.

This process can significantly improve their antioxidant response Kong et al. GSH is an endogenous antioxidant that exists in two forms in the human body, reduced thiol GSH and oxidized disulfide GSSG Raza, Depletion of GSH usually destroys the redox homeostasis of cells, leading to accumulation of ROS, which in turn triggers cell damage or even death Li X et al.

GST is involved in protecting DNA damage from oxidative stress by catalyzing the covalent binding of glutathione with hydrophobic and electrophilic substrates Hayes et al. The Alpha class GSTs can interrupt chain of lipid peroxidation reactions by reducing hydroperoxides and detoxifying the toxic end products of lipid peroxidation.

Sharma et al. The main function of SOD is to catalyze the dismutation of superoxide anion radical into O 2 and H 2 O 2. They have a significant effect on the treatment of atherosclerosis by reducing the peroxidation caused by the accumulation of free radicals and maintain the metabolic balance of the body Förstermann and Sessa, ; Li et al.

The primary role of CAT is to catalyze the decomposition of H 2 O 2 into H 2 O and O 2 , and protect cells from H 2 O 2 poisoning Wang Y et al. GPx is a GSH-dependent enzyme that converts reduced GSH to oxidized GSH, and simultaneously reduces lipid hydroperoxide to the corresponding lipid alcohol or free hydrogen peroxide to water Lubos et al.

NQO1 is a homodimer flavin enzyme that catalyzes the reductions of quinones to hydroquinones through obligatory 2-electron reductions. This obligatory two-electron reduction prevents the formation of semiquinone and superoxide or H 2 O 2 Dinkova-Kostova and Talalay, Reports have shown that EGCG can promote and mobilize the activities of a set of antioxidant enzymes in vivo , including GSH, SOD, CAT, GPX, and GST Na and Surh, Ramesh et al.

After treatment with acetaminophen N-acetyl-p-aminophenol, APAP , EGCG increased the activities of GSH and NQO In addition, the level of ROS, GSSG and TBARS in the liver decreased significantly.

EGCG also increased GPxs activity, which might be responsible for the decreased ROS production during APAP metabolism Yao et al. Polychlorinated biphenyls PCB can exacerbate oxidative stress in the body, and further induce inflammation of vascular endothelial cells.

Studies showed that exposure of vascular endothelial cells to PCB significantly increased superoxide. However, superoxide induced by PCB was significantly reduced when primary vascular endothelial cells were pretreated with EGCG.

Specifically, treatment of EGCG upregulated expression of antioxidant genes including GST and NQO1in a dose-dependent manner, all of which are controlled by NF-E2-related factor 2 Nrf2 Han et al. The Keap1-Nrf2-ARE pathway represents one of the most important cellular defense mechanisms against oxidative stress Bai et al.

Leucine zipper transcription factor a basic region of Nrf2 can activate ARE and start a variety of antioxidant reactions to prevent oxidative stress.

The Kelch-like ECH associated protein 1 Keap1 is a receptor that affects the expression of Nrf2. Without electrophiles or oxidants, Nrf2 is located in the cytoplasm and binds to Keap1 Kang et al.

The binding of Keap1 to Nrf2 results in ubiquitin dependent proteasomal degradation under basal reducing conditions. Under oxidative stress, stable Nrf2 translocates to the cell nucleus and forms a heterodimer with Maf.

It then interacts with ARE in target genes Magesh et al. Heme oxygenase 1 HO-1 is a strong antioxidant Araujo et al. It can increase the level of NO, reduce the level of inflammatory factors, reduce atherosclerotic plaque, and interfere with the formation and stability of plaque.

In addition, HO-1 regulates cholesterol transport and plasma lipid peroxidation Liu et al. Wu et al. found that after treatment with fixed concentration of 50 Amol EGCG, the level of HO-1 protein increased in a time-dependent manner.

An experiment found that endothelial cell cultures cotreated with EGCG plus actinomycin D AD or cycloheximide CHX were able to completely block induction by EGCG. AD and CHX are transcriptional and translational inhibitors respectively, suggesting that EGCG most likely induced HO-1 via de novo RNA and protein synthesis Wu et al.

Some catechin derivatives can oxidize the cysteine thiols of Keap1, which will form disulfide bonds and release the Nfr2 Na and Surh, For instance, under the influence of EGCG, the expression of Nrf2 decreased in cytoplasm and increased in the nucleus. Yu et al. found that ECG activated the Nrf2 and increased expression of HO-1 in ox-LDL induced VSMCs that previously had a very low expression of HO-1 and Nrf2 protein.

This implies that ECG significantly ameliorated the atherosclerotic damage of VSMCs Yu et al. Zheng et al. showed that after treatment with EGCG, nuclear accumulation of Nrf2 was significantly increased and the binding of Nrf2-ARE was also enhanced.

Lee and Kim, PPAR- a is an important target for the treatment of lipid metabolism disorder, because it can regulate the expression of many lipid related genes, Janssen et al. PPAR- γ regulates target genes downstream involved in lipid production, and promotes fatty acid transport and deposition Janani and Ranjitha Kumari, ; Xu et al.

EC attenuated the downregulation of PPARγ expression mediated by TNFα and reduced nuclear DNA binding Vazquez-Prieto et al. Similarly, studies have shown that EGCG can also restore the down-regulation expression of PPAR- γ Peng et al.

Therefore, EC and EGCG may act as PPAR-γ agonists to exert antioxidant effects. In addition, PPAR-γ coactivator-1α PGC-1α regulates genes involved in lipid metabolism and oxidative stress Bagattin et al.

It is also involved in the activation of PPARα Homologous. PGC1α and PPARα are key factors in antioxidant response Fracassi et al.

Research has proven that the activation of PPARα can trigger the activation of CAT, while PGC1α can regulate expression and localization of SOD2 and GPx1 Figuer 3 St-Pierre et al.

The use of EC rescued the decrease in level of PGC-1α, and exhibited beneficial effects on obesity and decreased relevant cardiometabolic risk factors Gutiérrez-Salmeán et al. Marinovic et al. demonstrated that EGC and EC can indirectly activate PPARα and reduce hepatic steatosis Marinovic et al.

Unfortunately, there are insufficient reports on the role of PPAR pathway in oxidative stress with catechins. Its role in ROS metabolism too has not been explored to a large extent. The MAPK mitogen-activated protein kinase signaling cascades involving MAPKs ERK extracellular signal regulated kinase , JNK c-Jun N-terminal kinase and p38 MAPK may play an important role in atherosclerosis and vascular restenosis Muslin, Inhibition of the cascade is believed to protect cells from oxidative stress.

Evidence suggests that when JNK, ERK, and p38 proteins are activated, ROS level increases, leading to oxidative stress and subsequently apoptosis Kong et al.

Specifically, the JNK pathway has been demonstrated to be part of oxidative stress responses in tumors, suggesting that inhibition of JNK signaling may be helpful to prevent several ROS-induced metabolic diseases Li C et al.

Activation of AP-1, a transcription factor, occurs through the MAPK pathway. Its activity is influenced by the intracellular redox environment, including the level of ROS and antioxidants Figuer 3 Higdon, J.

and Frei, B. EGCG can minimize the damage to endothelial cells and reduce IL-6 and TNF-α by inhibiting AP-1 activity Riegsecker et al. Catechins seem to inhibit AP-1 activity through inhibiting kinases in the MAPK pathway, such as JNK and Erks Katiyar et al.

EGCG was observed to significantly prevent thrombin-induced caspase 3 activation and apoptosis by suppressing JNK phosphorylation He et al. The molecular signaling pathway regulated by catechins is responsible for its pro-apoptotic and anti-proliferative characteristics.

One of which is the inhibition of a key oxidative stress-sensitive transcription factor -nuclear factor-κB NF-κB Khan and Mukhtar, ; Musial et al. After exposure to oxidative and inflammatory stimuli, I κ B kinase IKK is activated, leading to IKK signalsome phosphorylation, which are subsequently degraded by the proteasome.

Then NF-κB translocates to the nucleus, where it binds to specific promoter regions and initiates transcription. Karin, ; Surh, In addition, NF-κB may aggravate oxidative stress by influencing the Nrf2 signaling pathway.

Being a protein downstream of NF-κB, the research have shown that p65 may exert conflicting effects in the Nrf2 signaling pathway by accelerating peroxidation, leading to abnormal cell proliferation Figuer 3 Yang et al. Catechins, especially EGCG, can block the activation of NF-κB Varilek et al.

It was found that EGCG can reduce p65 expression induced by PCB polychlorinated biphenyls and down-regulate the expression of NF-κB regulated genes, further suppressing endothelial cells inflammation Liu et al. Many studies have proven that catechins are protective against AS and are effective natural antioxidants.

However, there are still a few limitations in place such as metabolite activity and low bioavailability.

Because catechins are rapidly and extensively metabolized, in vitro experiments data and the biological activity of catechins metabolites are often questioned. It is hence particularly important to demonstrate catechins antioxidant activity in vivo. Catechins have been found to experienced considerable biotransformation in vivo , and their main metabolic pathways are methylation, glucuronidation, sulfation and ring-fission metabolism.

Yang et al. EGCG metabolites and metabolites produced from EC or ECG are proven to have stronger free radical scavenging power than parental catechins Takagaki et al. The 30—and 40 -monomethyl ethers of EC can inhibit NADPH oxidase to increase NO in endothelial cells, thus reducing oxidative stress Steffen et al.

These evidence suggests that catechin metabolites can maintain the antioxidant capacity of their parent compounds. Another metabolic pathway includes the degradation of catechins.

Liver and intestine are the backbone of the metabolization and absorption of catechins Feng, Besides intestinal and liver metabolites, Sang et al.

also found metabolites in colon bacteria Sang et al. Investigation found that catechins not metabolized in the upper intestine were transported to the lower intestine through intestinal microflora Roowi et al.

Ottaviani et al. Therefore, there is great research potential in intestinal microbiota to improve production and hence the bioavailability of catechin metabolites. It is also important to continue studying the antioxidant effect of metabolites to find the optimal condition for catechins to play an antioxidant role better in the local intestinal.

Tea polyphenols are susceptible to degradation under environmental stresses or digestive circumstances, such as alkaline pH and high temperature. In addition, the low bioavailability of catechins also due to degradation and metabolism in the gastrointestinal tract, poor membrane permeability, and pre-systemic hepatic clearance Ye and Augustin, ; Sabaghi et al.

The development of new agents, such as nanoparticles, may become an effective way to solve this problem in the future. Recently, studies found that nanomaterials based on carbon, nanozymes, and nanomedicine could improve stability of antioxidant treatments and further upgrade the antioxidant effect.

For instance, nitrogen-doped carbon nanodots ionogels Rizzo et al. Green nanoparticles GNPs prepared by Yang et al. using TP in green tea as the monomer have strong free radical scavenging ability and oxidation resistance.

The research provides a new green strategy for making safe and effective antioxidants. It has been reported that synergistic effects of the combination of EGCG and fish oil. The presence of fish oil increased the bioavailability of EGCG Giunta et al.

Furthermore, using broccoli byproducts as the matrix for co-delivery of EGCG and fish oil could prevent the degradation of EGCG in the upper gastrointestinal tract can thus be metabolized by the microorganisms in the lower gut, leading to an increase in EGCG bioavailability Shi et al.

In addition, the combination of catechins with other drugs that show synergistic effects may be a promising approach, such as catechins showing good synergy with some conventional anticancer drugs Cai et al.

Moreover, under certain conditions, catechins may have both prooxidative or toxic effects. The dual antioxidant and pro-oxidant functions of catechins depend primarily on the dose level and the biological context. Some European regulators have suggested that the tolerable upper intake level of EGCG should be mg per day for humans Yates et al.

Tian et al. found that at 0. It is possible to optimize the TP level of foods or beverages based on emulsion to achieve the best antioxidant activity Tian et al.

With the aging of the general population and the increase in chronic diseases such as hypertension and diabetes, the incidence rate of atherosclerosis further increase. Atherosclerosis has no obvious early symptoms.

When the disease progresses to a higher stage with age, symptoms of atherosclerosis will appear. Therefore, it is very important to seek preventive diet or drugs, and the strategy of prevention before disease will greatly reduce hospital costs and other economic burdens of patients.

The development of natural products to prevent AS has scientific significance and application value. At the same time, the discovery of lipid oxidation products implies that oxidative stress promotes the change of lipid metabolism, which provides a new idea for the treatment of diseases with abnormal lipid metabolism.

Tea, especially unfermented green tea, is rich in catechins, which have antioxidation and improve lipid metabolism disorders. The health benefits of tea are largely attributed to the effects of catechins. However, catechins correspond to a variety of targets and act through different signaling pathways.

Due to the pleiotropic effects of catechins, more definitive studies on their biological functions and anti-atherosclerotic mechanisms are lacking before their clinical application. Current studies have not systematically revealed the mechanism of catechins in anti-oxidative stress to regulate abnormal lipid metabolism in AS.

Therefore, we hope to clarify the therapeutic effect of catechin in AS by combing the mechanism of catechin regulating oxidative stress and improving abnormal lipid metabolism.

This study will provide a reference for the subsequent development of catechin as AS adjuvant drugs. Catechins play an antioxidant role in many ways, namely, by balancing enzyme activity and regulating signal pathways.

They inhibit NADPH oxidase, XO, COX2, NOS, and other enzymes that produce ROS and activate antioxidants in the body, such as GSH, SOD, CAT, GPX, GST, NQO1, to significantly improve the antioxidant response. These reactions all work together to help reduce oxidative stress. It is noteworthy to point out that there are still many limiting factors for the application of catechins, such as prooxidative and toxic effects under certain conditions, the dubious activity of its metabolites and low bioavailability.

Determining the safe dose of catechin and finding the biological environment that can exert the best antioxidant activity of catechin are effective methods to overcome the pro-oxidative side effects of catechin.

Promoting the catabolism of catechins by intestinal flora can enhance the absorption and utilization of the host. Isolation and identification of microorganisms and microbial metabolites with the ability to catabolize the active catechins may be one of the methods to improve the utilization of catechins.

The development of new preparations of catechins based on nanomaterials greatly improves their antioxidant stability. The combination of catechin with other bioactive dietary compounds and disease treatment drugs can play a synergistic effect of promoting the absorption and utilization of both sides.

All these provides a new idea for solving the problem of low bioavailability of catechins. Current research on catechins focuses on functional and metabolic studies. In the future research, the physiological function of catechins can be combined with their chemical structure and in vivo process.

More clinical trials can be carried out to further verify the role of catechins in the prevention and treatment of AS. Studies on the pharmacokinetics and pharmacodynamics will be the focus of the application of catechins in AS. In order to improve the clinical application of catechins, the combination of catechins with existing AS drugs may become a direction of research on AS treatment.

The potential combination of pharmaceutical and nutritional levels is able to establish a more effective treatment regimen. More researches are needed to elucidate the antioxidant mechanism of catechins.

Despite its limitations, we can effectively conclude that regular intake of an appropriate amount of tea can regulate the antioxidant capacity of the human body, improve lipid metabolism, and hence prevent atherosclerosis. YuS, YiS, and YT lead the conception and design of the manuscript.

YuS and YiS drafted the manuscript and figures. YuS, YiS, YY, and JW collected and interpreted the relevant literature. FZ, YL, YT, and YaS contributed to the provided guidance of the whole manuscript and reviewed the manuscript. All the authors of the article has made a contribution, and approved the version submitted.

We are grateful for funds supported from the National Natural Science Foundation of China Grant No The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher.

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Zillich OV, Schweiggert-Weisz U, Hasenkopf K, Eisner P, Kerscher M. Release and in vitro skin permeation of polyphenols from cosmetic emulsions. Download references. We would like to thank Yeoju-si and Yeoju Institute of Technology Gyeonggi-do, Republic of Korea for their support for this study.

Department of Cosmetics Engineering, Graduate School of Konkuk University, Neungdong-ro, Gwangjin-gu, Seoul, , Republic of Korea.

Department of Beauty Art, Doowon Technical University, Jurawui-gil, Paju-eup, Paju-si, Gyeonggi-do, , Republic of Korea. Department of Beauty Yakson Care, Yeoju Institute of Technology, Sejong-ro, Yeoju-si, Gyeonggi-do, , Republic of Korea.

You can also search for this author in PubMed Google Scholar. JB, NK, YS, and YJK designed the study and analyzed data, and JB, NK, YS, SYK, and YJK wrote the manuscript and figure together. All authors read and approved the final manuscript.

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Search all BMC articles Search. Download PDF. Download ePub. Abstract Background Catechins, which are polyphenol compounds found in many plants and are an important component of tea leaves, are strong anti-oxidants.

Research Many studies seek to enhance the effects of catechins on the human body and boost their protective power against UV radiation.

Conclusion Continued research on the strong anti-oxidant effects of catechins is expected to result in many advances in the food, cosmetics, and pharmaceutical industries.

Background Catechins have many benefits including preventing or reducing skin damage. Full size image. Conclusions Table 1 summarises the activities of catechins and their applications. Table 1 Activities of catechins and their applications Full size table.

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For more Targeted weight control about PLOS Subject Antii-nflammatory, click here. Green tea digestion inflammation is a fundamental symptom Anti-imflammatory many diseases. Catechin catecnins anti-oxidant and Green tea digestion properties. However, the mechanism of catechin to prevent inflammation in 3T3-L1 adipocytes caused by TNF-α remains unknown. Therefore, the effects of catechin on the gene expression of cytokines and the activation of cell signals in TNF-α induced 3T3-L1 adipocytes were investigated. The effects of catechin on adipogenesis and cell viability were detected by Oil Red O staining and CCK-8 assay, respectively. The genes expression of cytokines was determined by real-time RT-PCR.

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