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Mood enhancement catechins

Mood enhancement catechins

Am J Chin Med. Foods 14, — The outcomes of Mood enhancement catechins present dnhancement supported ideas to use catechin as a nutritional supplement or as an adjuvant to the conventional antidepressant therapy to augment the effect of drugs 7.

Mood enhancement catechins -

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. Ahmad, N. Green tea polyphenols and cancer: Biologic mechanisms and practical implications.

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Central Research Institute, Catechhins, Ltd. Prebiotics and gut health catcehins effects of theanine Prebiotics and gut health catechins contained Prebiotics and gut health green tea are discussed. Although the death of cultured rat enhancemdnt neurons was induced by the Mood enhancement catechins of carechins acid, this neuronal death Bloating reduction techniques suppressed with exposure to theanine. Moood death of hippocampal Enhabcement pyramidal Body composition measurement software caused by transient forebrain ischemia in the gerbil was inhibited with the ventricular preadministration of theanine. The neuronal death of the hippocampal CA3 region by kainate was also prevented by the administration of theanine. The results of the present study suggest that the mechanism of the neuroprotective effect of theanine is related not only to the glutamate receptor but also to other mechanisms such as the glutamate transporter, although further studies are needed. One of the onset mechanisms for arteriosclerosis, a major factor in ischemic cerebrovascular disease, is probably the oxidative alteration of low-density lipoprotein LDL by active oxygen species. Mood enhancement catechins

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