In one large-scale clinical High-quality content creation Alpha-lipoic acid for brain health compared effectts tea drinkers with nondrinkers Grefn found that those who drank the most tea were less likely to develop pancreatic cancer. LPS activated toll-like receptor TLR-4 expression and induced innate immune response leading to uveitis Popular articles. Ryu OH, Lee J, Lee KW, et al.

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Green tea extract and anti-inflammatory effects -

As a result, these supplements may contain other substances that are unsafe for health or have unproven health benefits. Further research is necessary to determine the best time to drink green tea.

However, since green tea contains caffeine, some people may prefer to drink it in the morning. Research suggests it is safe for most adults to drink up to 8 cups of unsweetened green tea daily. However, people should be aware of the amount of caffeine in the brand they choose.

Some research suggests that regular tea consumption, including green tea, may help to reduce body weight and waist-to-hip ratios. However, several factors can influence fat loss, including total calorie intake and exercise levels. Green tea may have several health benefits. For example, it may help with weight management, skin inflammation, and type 2 diabetes.

Some research also links green tea consumption to improved cardiovascular health. Green tea has one of the highest concentrations of antioxidants of any tea. It is naturally low in calories and contains less caffeine than black tea and coffee. Most people can drink green tea daily with no side effects.

However, some people may experience sleep disturbances due to the caffeine in green tea if they drink large amounts or consume it late in the day. Do you enjoy tea for its flavor or the soothing feeling brought by holding a steaming cup?

In this Spotlight, we tell you which brews are best for…. Matcha is a green tea powder that people tend to use in traditional tea ceremonies.

Modern uses include flavoring smoothies, cakes, and lattes. It may…. Some studies have shown that caffeine can benefit overall health. However, others suggest that it may be harmful in excess. Read more to find out….

What are micronutrients? Read on to learn more about these essential vitamins and minerals, the role they play in supporting health, as well as….

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Medical News Today. Health Conditions Health Products Discover Tools Connect. What are the health benefits of green tea? Medically reviewed by Jared Meacham, Ph. Cancer prevention Weight loss Skin conditions Heart health Lower cholesterol Stroke risk Type 2 diabetes Memory Alzheimer's disease Other benefits Nutrition Types Side effects FAQ Summary People have hailed the health benefits of green tea for centuries.

Cancer prevention. Weight loss. Inflammatory skin conditions. Heart health. Lower cholesterol. Stroke risk. Type 2 diabetes. Working memory. The bold plasma metabolites in the tables indicate that those metabolites give higher correlation coefficients and have wider coverage to the metabolites present in the retina.

Phospholipase A2 PLA2 hydrolyses the sn-2 position of membrane and plasma glycerophospholipids to release arachidonic acid which is a precursor of eicosanoids such as prostaglandins and leukotrienes for inflammation actions. It also produces lipid mediators like lysophospholipids. The relative PLA2 activities in plasma in the LPS group were Figure 5 The proposed mechanism of how catechins in GTE inhibit phospholipase A2 PLA2 activity and alleviate retinal inflammation and metabolic stress.

A The chart shows the relative PLA2 activities in six rat plasma samples of different treatment groups. B LPS induced fever caused by LPS induced PLA2 activity to increase lipid digestion and subsequently reduce phosphocholine lipids. Catechins inhibited PLA2 activity, increased PC levels, and subsequently inhibited inflammation.

Inflammation of the iris in our EIU model and the anti-inflammatory effects of GTE treatment were consistent with our previous study 2. In chronic ocular inflammation, neuritis has been reported to detriment neuron conductivity and diminish evoked potential However, in our EIU model of acute ocular inflammation, the conductivity was not affected as shown by ERG in the a- and b-waves.

GTE could improve the sensory symptom but not the conductivity of the nerve 27 through anti-oxidation protection In our study, the conductivity of the rod photoreceptors and bipolar cells was improved by GTE treatment Figure 1D , suggesting temporary increase of conductivity by GTE.

Our results showed different systemic and retinal metabolic responses to the LPS induced inflammation and subsequent GTE alleviation. The systemic metabolic responses to LPS included increases in inflammation promoting prostanoids, inflammation resolving corticosteroids, bile acids, endogenous antioxidants, and degraded peptides.

There were decreases in structural and signal related lipids and fatty acids, and basal metabolic regulatory hormone thyroid hormone tyrosine. The inflammation was so intensive that 5-hydroperoxide 5-HPETE , a precursor of leukotriene, was exhausted Supplementary Figure 2.

The systemic metabolic responses of GTE on LPS induced inflammation included increases in structural and signal related lipids and fatty acids but decreases in inflammation associated prostanoids, bile acids, and degraded peptides.

Similarly, the retinal metabolic responses to LPS included increase of energy associated vitamins, co-factors, and metabolites of neurotransmitters but decreases of anti-inflammation related corticosteroids and histamine metabolites, signaling related phospholipids and nucleotide metabolites.

The retinal metabolic responses of GTE on LPS induced inflammation included increases in signaling nucleotides metabolites but decreases in structural and signaling related lipid and fatty acid mediators, inflammation associated prostanoids, and energy-related vitamins and co-factors Figures 2 , 3.

Taken together, the results suggested that GTE relieved different metabolic and energetic stresses, and resolved structural destruction and toxicity.

Pathway analysis also showed that LPS activated systemic metabolic inflammatory-related pathways, prostaglandin biosynthesis, leukotriene metabolism, and steroid hormone biosynthesis.

LPS caused homeostatic responses to release corticosteroids to counter inflammation. In the retina, it activated inflammation pathways, caused protein degradation, and disturbed energy production metabolisms by increased vitamin B5 but decreased vitamin B6, fructose and mannose metabolisms pathways.

It also suppressed pathways involving selenoamino acid metabolism to reduce antioxidant capacity and caused oxidative stress.

GTE relieved systemic inflammation by suppressing systemic inflammation-related pathways that involved arachidonic acid metabolism and activating cellular signaling glycerophospholipid metabolism.

In the retina, it relieved inflammation by activating signaling pathways like the glycosphingolipid biosynthesis pathway and suppressing prostanoid production and glycerophospholipid biosynthesis for membrane signaling Supplementary Table 2.

Significant differentiated metabolite profiles in the plasma were found following LPS induction and after GTE treatment.

Phosphorylcholine lipids have anti-inflammatory property and inhibited TNF-α-mediated NF-κB translocation in a dose-dependent manner in Caco-2 cells Classical eicosanoids from COX mediated metabolites of arachidonic acid and N-acylamides, N-palmitoyl proline, are strongly pro-inflammatory LPS modulates phosphorylcholine lipid, arachidonic acid metabolites, N-palmitoyl proline, thyroxine, and nutriaholic acid, which are associated with inflammation responses 31 , 32 , basal metabolism, hepatic detriment 33 , 34 , and signaling Alanylglutamine can reduce infection-induced inflammatory damage, and infection-associated symptoms like dehydration, and inhibits apoptosis due to cellular damage LPS induced homeostatic responses to increase corticosteroids, alanylglutamine, and DL-α-lipoic acid are associated with immune responses 37 , 38 , mitochondria stress suppression 33 , and anti-oxidation recovery 39 Figure 2E Supplementary Table 1A.

After GTE treatment, it increased phosphorylcholine lipids but lowered free structural lipids, arachidonic acid metabolites, bile acid metabolites, 7alpha-hydroxyoxo-5b-cholanoic acid, and acyl glycine, glutarylglycine, which is associated with mitochondrial fatty acid beta-oxidation as acylglycines, are normally minor metabolites of fatty acids, indicating inflammation was relieved, cellular membrane integrity maintained, hepatic recovered and mitochondria stress relieved Figure 2F Only polyphenol catabolite, acetoxytoxol, was detected in plasma suggesting extensive metabolism of catechins whose direct anti-inflammatory effects are thus questionable Supplementary Table 1B.

In the retina, LPS lowered the histamine antagonist, ethanolamine and the endogenous antioxidant se-methylselenocysteine but increased the glucocorticoid noraldosterone, the catabolite monodehydroascorbate 41 , 42 and tissue damaged associated metabolites, N-acetylglucosamine 6-sulfate and L-alpha-glutamyl-l-hydroxyproline.

Homeostatic response increased the absorption of L-ascorbate 6-phosphate, elevated 7-aminomethylcarbaguanine and D-pantothenoyl-L-cysteine 43 , But it depleted inflammation mediators, fucosephosphate, and energy sources, D-Glucosephosphate 45 , increased membrane signaling lipid metabolites, metabotoxin, adipic acid 46 , and increased amino acid precursor, Rmethylmalate.

Neuron activity was compromised as the reduction of neural peptide, N-acetylaspartylglutamic acid, amino acid, aminolevulinic acid, and increasing the melanocytes and neurotransmitters metabolites, cysteinyldopa and pyrocatechol 47 , These findings indicate inflammation; oxidative, mitochondrial and retinal stress; and tissue damage have occurred with the activation of energy production and biosynthesis pathways Supplementary Tables 1C, D Figure 3E.

After GTE treatment, the metabolites profiles in the retina also showed inflammation resolved. GTE reduced the inflammatory prostaglandin metabolite tetranor-PGAM and lowered free glycerophosphocholine level It also decreased the collagen degradant L-alpha-glutamyl-l-hydroxyproline, elevated the selenium antioxidant 1β-methylseleno-N-acetyl-D-galactosamine, decreased antioxidant amino acid metabolites, N-acetyl-L-methionine and energy production associated metabolites, D-pantothenoyl-L-cysteine, and lowered 2-ethylacrylcarnitine and kynuramine.

But it increased signaling cyclic CMP L-Carnitine transports fatty acids into the mitochondrial matrix to produce energy. L-carnitine and its esters metabolites increased during oxidative stress Kynuramine is a biogenic amine, which is a major metabolite of melatonin in the brain produced by oxidative and photochemical reactions.

Therefore, they can be a biomarker for oxidative stress and inflammation It indicates relief of inflammation and oxidative, mitochondrial, and neuronal stress with recoveries of membrane integrity, cellular activities, and biosynthesis.

Correlation of the metabolites in the plasma with the retina showed the highest correlated systemic metabolites to retinal metabolites were phosphorylcholine lipids, fatty acids, and arachidonic acid metabolites Figure 4 Supplementary Table 3.

The phosphorylcholine lipids involve immune regulation and maintenance of tissue homeostasis. Bioactive endogenous lipids are important mediators in all phases of inflammation involving regulation, fine-tuning, and cessation.

While classical eicosanoids are mainly pro-inflammation, some lysoglycerophospholipids and sphingolipids are pro-resolving mediators.

Phosphatidylcholine PC also showed anti-inflammatory properties against TNF-α induced inflammation in ulcerative colitis 29 , 31 , LPS caused both ocular and systemic inflammation possibly by suppressing phosphorylcholine lipids production. The systemic levels of phosphatidylcholine and lysophosphatidylcholine were correlated with retinal metabolites.

On the other hand, GTE increased systemic phosphatidylcholine and sphingosine metabolite, N-stearoyl serine, were negatively associated with retinal metabolites relating to the malfunction of mitochondria, neuron stress, tissue damage, and inflammation Figure 4B 54 , LPS activated toll-like receptor TLR-4 expression and induced innate immune response leading to uveitis Phospholipids decreased activation of TLR-4 by competitive interaction with accessory proteins of TLR-4 PLA2 increased lipid digestion and reduced absorption of phosphatidylcholine and lysophosphatidylcholine 58 , Catechins inhibited PLA2 and could increase phosphatidylcholine and lysophosphatidylcholine levels and decrease the arachidonic acid AA , a precursor of eicosanoid metabolites, to release for anti-inflammation In this study, LPS lowered the systemic phosphocholine lipid level and indirectly induced inflammation in the retina.

GTE could then inhibit TLR-4 activity indirectly by increasing the systemic phospholipid and sphingosine levels Figure 5. In our metabolomic study, GTE alone was not used as a control because it affects many metabolic pathways This study aimed to investigate the underlying metabolic mechanisms how GTE can resolve the inflammation induced by LPS, so GTE with LPS served as treatment controls while LPS as a positive control.

However, this study is an untargeted metabolomics study. Although we have verified the identity of the metabolites according to the exact mass and fragmentation patterns, we need to do targeted metabolomics to further confirm the identity of each metabolite.

Since many metabolites are not commercially available, we cannot perform a comprehensive targeted metabolomics analysis in this study. Nevertheless, we plan to select a few target phospholipids for further studies and validation.

The untargeted metabolomics approach can overview a series of underlying mechanisms of LPS caused inflammation and GTE alleviation simultaneously. It showed LPS induced inflammation involved signaling suppression, oxidative and respiratory stress, and increased energy consumption in the retina.

GTE relieved the inflammation was associated with alleviating oxidative, mitochondrial, and neuronal stresses, and energy consumption. GTE may increase systemic phospholipids to alleviate ocular inflammation indirectly rather than act directly with anti-inflammatory effects on the retina tissues.

Phospholipids could be a potential therapeutic agent for ocular inflammation. Further inquiries can be directed to the corresponding author.

The animal study was reviewed and approved by the Animal Ethics Committee of the Chinese University of Hong Kong. Written informed consent was obtained from the owners for the participation of their animals in this study.

KOC: conceptualization, methodology, validation, formal analysis, investigation, data curation, writing - original draft, writing - review and editing, visualization, supervision, and project administration; KPC and YY: methodology and investigation; WC: writing - review and editing; CW: review and editing, funding acquisition; CP: writing — review and editing, supervision, resources, and funding acquisition.

All authors contributed to the article and approved the submitted version. The study was funded by Research Grant Council General Research Fund Project 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.

Musial C, Kuban-Jankowska A, Gorska-Ponikowska M. Beneficial Properties of Green Tea Catechins. Int J Mol Sci doi: CrossRef Full Text Google Scholar. Qin YJ, Chu KO, Yip YW, Li WY, Yang YP, Chan KP, et al. Green Tea Extract Treatment Alleviates Ocular Inflammation in a Rat Model of Endotoxin-Induced Uveitis.

PLoS One 9:e PubMed Abstract CrossRef Full Text Google Scholar. Durrani OM, Tehrani NN, Marr JE, Moradi P, Stavrou P, Murray PI. Degree, Duration, and Causes of Visual Loss in Uveitis. Br J Ophthalmol — Gritz DC, Wong IG.

Incidence and Prevalence of Uveitis in Northern California; the Northern California Epidemiology of Uveitis Study. Ophthalmology — Siddique SS, Shah R, Suelves AM, Foster CS.

Road to Remission: A Comprehensive Review of Therapy in Uveitis. Expert Opin Investig Drugs — Pavesio CE, Decory HH. Treatment of Ocular Inflammatory Conditions With Loteprednol Etabonate.

Br J Ophthalmol 92 4 —9. Becker B, Mills DW. Elevated Intraocular Pressure Following Corticosteroid Eye Drops. JAMA —6. Jabs DA, Rosenbaum JT, Foster CS, Holland GN, Jaffe GJ, Louie JS, et al. Guidelines for the Use of Immunosuppressive Drugs in Patients With Ocular Inflammatory Disorders: Recommendations of an Expert Panel.

Am J Ophthalmol — Ren JL, Yu QX, Liang WC, Leung PY, Ng TK, Chu WK, et al. Green Tea Extract Attenuates LPS-Induced Retinal Inflammation in Rats. Sci Rep Li J, Yip YWY, Ren J, Hui WK, He JN, Yu QX, et al.

Green Tea Catechins Alleviate Autoimmune Symptoms and Visual Impairment in a Murine Model for Human Chronic Intraocular Inflammation by Inhibiting ThAssociated Pro-Inflammatory Gene Expression.

Rosenbaum JT, McDevitt HO, Guss RB, Egbert PR. Endotoxin-Induced Uveitis in Rats as a Model for Human Disease. Nature —3. Howes EL Jr, Aronson SB, McKay DG. Ocular Vascular Permeability. Effect of Systemic Administration of Bacterial Endotoxin. Arch Ophthalmol —7.

Kogiso M, Tanouchi Y, Mimura Y, Nagasawa H, Himeno K. Endotoxin-Induced Uveitis in Mice. Induction of Uveitis and Role of T Lymphocytes. Jpn J Ophthalmol — PubMed Abstract Google Scholar. Bhattacherjee P, Williams RN, Eakins KE. An Evaluation of Ocular Inflammation Following the Injection of Bacterial Endotoxin Into the Rat Foot Pad.

Invest Ophthalmol Vis Sci — Moita E, Gil-Izquierdo A, Sousa C, Ferreres F, Silva LR, Valentão P, et al. Integrated Analysis of COX-2 and iNOS Derived Inflammatory Mediators in LPS-Stimulated RAW Macrophages Pre-Exposed to Echium Plantagineum L.

Bee Pollen Extract. PloS One 8:e Kozak YD, Omri B, Smith JR, Naud MC, Goldenberg BT, Crisanti P. Protein Kinase Cζ Pkcζ Regulates Ocular Inflammation and Apoptosis in Endotoxin-Induced Uveitis EIU.

Am J Pathol — Ruiz-Moreno JM, Thillaye B, de Kozak Y. Retino-Choroidal Changes in Endotoxin-Induced Uveitis in the Rat. Ophthalmic Res —8. Chu KO, Chan SO, Pang CP, Wang CC. We have previously shown epigallocatechingallate EGCG is the most biologically active constituent of catechins in green tea extract GTE.

In this study we determine the anti-inflammatory effects of GTE, catechin mixtures and EGCG alone on endotoxin-induced uveitis EIU in Sprague Dawley SD rats.

Twenty four hours after injection, the eyes were examined by slit-lamp prior to terminating the animals for collection of aqueous humors for cell count and protein assay or enucleation of eyeballs for immunohistochemistry.

LPS caused severe hyperemia and edema in the iris, substantial accumulation of infiltrated cells and total protein in the aqueous humor.

Our data showed that GTE and its catechins combination exhibited a potent anti-inflammatory action in an experimental model of acute ocular inflammation. Further experimentations are being done to investigate whether more potent therapeutic action is obtained at lower dosages and with different combinations of catechins.

Purchase this article with an account. Jump To ARVO Annual Meeting Abstract April Green tea extract as a multiple compound is the most potent anti-inflammatory agents in endotoxin-induced uveitis. Yongjie Qin ; Kai On Chu ; Yolanda Wong Ying Yip ; Wai Ying Li ; Sun On Chan ; Chi Pui Pang.

Commercial Relationships Yongjie Qin , None; Kai On Chu , None; Yolanda Wong Ying Yip , None; Wai Ying Li , None; Sun On Chan , None; Chi Pui Pang , None.

Effcts Green tea anti-inflakmatory been shown to have aanti-inflammatory effects Snti-inflammatory a variety of diseases such Anti-cancer therapies cancer, obesity, diabetes, cardiovascular disease, and neurodegenerative diseases. Through cellular, animal, and human experiments, green tea and Green tea extract and anti-inflammatory effects major component, epigallocatechingallate EGCG have extraxt demonstrated Extraxt have anti-inflammatory effects. We also reviewed results from cellular and animal experiments and proposed action mechanisms. Results: Most of the results from the human studies indicated the beneficial effects of green tea and tea catechins against inflammatory diseases. Conclusion: Since green tea and EGCG have multiple targets and act in a pleiotropic manner, we may consider their usage to improve the quality of life in patients with inflammatory disease. Green tea and EGCG have beneficial health effects and no severe adverse effects; however, care should be taken to avoid overdosage, which may induce deleterious effects including hepatic injury. People have antii-inflammatory the health benefits of Preventing premature aging tea for centuries. Studies ahd that consuming green tea may extrzct affect Green tea extract and anti-inflammatory effects health, help with weight Beta-carotene in pumpkins, and reduce the risk of cardiovascular disease, among other benefits. Green tea comes from unoxidized leaves of the Camellia sinensis bush. It is one of the least processed types of tea, containing the most antioxidants and beneficial polyphenols. However, more evidence is necessary for researchers to definitively prove these health benefits.