Green tea extract and eye health -
However, the need for long-term use, the presence of preservatives and concomitant use of multiple classes of topical anti-glaucoma medication increase the risk of developing ocular surface disease For example, benzalkonium chloride was found to cause conjunctival inflammation and epithelial toxicity To treat these ocular surface diseases, many therapeutic targets in the inflammatory cascade have been identified for ocular surface inflammation.
Topical use of cyclosporine 39 and lifitegrast 40 targeting the inflammatory components are available in clinical practice to manage dry eye. Teas can be categorized into non-fermented green tea, semi-fermented oolong tea, and fermented black tea, according to various manufacturing processes.
Green tea is the non-fermented leaves of plant Camellia Sinensis. Green tea preserves the natural structure of green tea polyphenolic constituents due to the initial stages of manufacturing. Green tea polyphenols include catechins, anthocyanins, flavones, and phenolic acids.
To obtain green tea extract GTE , fresh leaves have to go through complicated manipulations in laborious and well controlled extraction procedures.
Among these green tea catechins, EGCG has been demonstrated to be bioavailable and could target the molecular pathways in multiple disease models 42 — It is also the most potent components in terms of biological activities among green tea catechins.
The chemical structures of green tea catechins are shown in Figure 2. The chemical structure of polyphenols is characterized by the presence of several hydroxyl groups on different sites of a carbon atom, which may interact with reactive oxidizing species hence inhibiting oxidative stress.
Thus, the antioxidant activity of green tea is strongly associated with the electron-rich properties of polyphenols. The 2,3-double bond and the unsaturated 4-oxo group in the C-ring facilitates electron delocalization of o-dihydroxyl catechol within the B-ring Figure 2.
Chemical structures of eight green tea catechins The biological activities of catechins are well-known and their antioxidant, anticancer, anticardiovascular, antiobesity and antidiabetic properties have been widely documented In this review, we shall discuss the effects of green tea extracts on autoimmune uveitis, endotoxin-induced uveitis, oxidative-induced retinal degeneration, glaucoma, ocular surface inflammation and systemic inflammatory diseases Figure 3.
Figure 3. Multiple functions of GTE in various ocular and systemic inflammatory diseases. There are few animal studies investigating the uptake and distribution of green tea catechins in ocular tissues and fluids in rats through oral administration.
documented the differential distribution of catechins in various eye tissues GTE was highly concentrated in retina and aqueous humor.
The time to reach maximum concentration of GTE after ingestion varied in different tissues ranging from 0. A further study by the same group revealed that EC, EGC and EGCG were dominant in various ocular tissues except vitreous humor, where GC was predominant In another study of feeding GTE to pregnant rats, catechins could be detectable at higher concentrations in fetal eyes than in other fetal organs including brain, lung, heart, liver, and kidney Currently, important findings of numerous basic immunological mechanisms and novel therapies in autoimmune uveitis have been revealed by animal studies based on the mouse models of experimental autoimmune uveoretinitis EAU 51 — Previously, to objectively evaluate the therapeutic effects of anti-inflammatory agents in EAU mice, we developed a novel evaluation system consisting of three quantitative indicators, which are retinal-choroidal thickness RCT , major retinal vessel diameter and electroretinography ERG amplitudes We advocate these live measurements.
Objective and more reliable evaluations could be made because the same animals can be followed with the equipment repeatedly. Also less animals are needed for follow-up studies, which make the investigations more ethical.
These evaluations are more clinically relevant as similar tests are also regularly performed in human. We investigated the therapeutic effects of GTE and EGCG in the EAU model After oral administration of GTE, EGCG, dexamethasone, or water, our quantitative evaluation found that GTE, but not EGCG, was able to attenuate several inflammatory signs, including clinical manifestations, histopathological ocular damages, retinal-choroidal edema and retinal vasodilation, in EAU eyes.
Therefore, besides EGCG, other catechins and components in GTE may also play roles in EAU alleviation. Interestingly, GTE, as well as high dose EGCG, helped to maintain visual function, which impaired by inflammation in EAU mice.
IL-1β and IL-6 are critical factors in determining the lineage choice of differentiating Th17 cells. ILA and TNF-α are the hallmark pathogenic cytokines produced by Th17 cells Administration of anti-IL-1β or anti-IL-6 antibody has been shown to attenuate EAU in mice 60 , 61 and humans Based on the quantitative results of our studies, GTE and EGCG effectively downregulated the IL-1 β , IL-6, ILA , and TNF- α expression in retinal tissues from EAU mice, suggesting GTE and EGCG could inhibit EAU by targeting the Thassociated pro-inflammatory gene expression.
Remarkably, GTE treatment showed comparable improvements to the standard dosage of dexamethasone administration in most of the disease phenotypes, or even better in remissions of clinical inflammatory manifestations, vasodilation, and TNF- α expression.
EGCG showed less effective alleviation of EAU comparing with dexamethasone Qin et al. investigated anti-inflammatory effects of GTE on endotoxin-induced uveitis EIU EIU can be induced by systemic injection of lipopolysaccharide LPS , mimicking the pathological conditions in human infectious uveitis LPS produced severe hyperemia and edema in the iris.
Immunocytochemical examinations showed an accumulation of infiltrating cells in the aqueous humor that were immunopositive for cluster of differentiation 43 CD43 and CD68, which are markers for leucocytes and macrophages, respectively.
Analyses of the aqueous humor showed an increase in pro-inflammatory mediators including tumor necrosis factor-alpha TNF-a , interleukin-6 IL-6 and monocyte chemoattractant protein-1 MCP GTE treatments improved the clinical manifestations and reduced infiltrating cells and protein exudation in the aqueous humor in a dose-dependent manner.
The number of CD68 positive macrophages residing in the iris and ciliary was also reduced. GTE suppressed the production of TNF-a, IL-6 and MCP-1 in the aqueous humor, which was associated with a down-regulation of LPS receptor complex subunits, Toll-like receptor 4 TLR-4 and CD14, and suppression of nuclear factor kappa B p65 NFkBp65 in the iris and ciliary bodies.
Our findings show that GTE is a potent anti-inflammatory agent against the inflammation of EIU, suggesting a potential use in treating acute uveitis. Several studies have been conducted to explore the anti-oxidative effects of GTE and EGCG in age-related macular degeneration AMD.
Previous studies found that genetic polymorphism in CFH , an important regulator of the complement system in innate immunity, is associated with AMD 28 , In another study, Zhang et al.
induced the oxidative damages in retinal photoreceptors by intraocular injection of sodium nitroprusside Visual function assessed by ERG a- and b-wave amplitudes showed significant reductions after the injection.
Decreased expression of photoreceptor-specific markers RET-P1 and rhodopsin kinase and increased cell death marker caspase-3 were demonstrated by RT-PCR and Western blotting after the injection of sodium nitroprusside.
Interestingly, EGCG co-injection with sodium nitroprusside significantly blunted these detrimental effects in the retina. Chronic inflammation could be induced by oxidative stress Yang et al.
investigated the anti-oxidative action of GTE in another animal model of oxidative stress specifically to the retina They induced oxidative degeneration of retina in rats by intravenous injection of sodium iodate.
In vivo imaging by cSLO and SD-OCT observed the pathological changes of the retina, especially in the inner nuclear layer, outer nuclear layer and retinal pigment epithelial layer, caused by sodium iodate.
Based on the imaging technology, they found the retinal lesions were significantly ameliorated by GTE. Further analyses of oxidative stress markers revealed reduced expression of superoxide dismutase, glutathione peroxidase, caspase-3 and 8-iso-prostaglandin F2α.
Choroidal neovascularization CNV is a key feature in the neovascular subtype of AMD. Laser photocoagulation could be employed to induce CNV in animals. Recently, a study showed that oral feeding of a prodrug of EGCG pro-EGCG could significantly reduce the CNV area and vessel leakage in the laser treated mice EGCG has unfavorable bioavailability due to its lower stability in neutral or alkaline conditions in intestines.
Also EGCG is hydrophobic which would interfere with its absorption Pro-EGCG can improve the stability and bioavailability of EGCG through acetylation of its reactive hydroxyl groups.
Cellular esterase can convert pro-EGCG into EGCG In conclusion, this study showed that EGCG could reduce CNV and suppress inflammation in a wet AMD animal model.
In a similar study, light-induced photoreceptor degeneration was alleviated by intraperitoneal injection of EGCG In these animals, cone b wave, and rod a and b waves were all significantly improved after EGCG injection.
The expression of antioxidant gene Sod2 was also rescued in EGCG injected animals. Our metabolomic study in human umbilical-vein endothelial cells HUVECs found that GTE could exert its anti-angiogenic properties through suppressing synthesis of cellular building blocks and oxidative-phosphorylation metabolites, while promoting the synthesis of membrane lipids and growth factors In another study, polysaccharides purified from GTE was shown to protect human retinal pigment epithelial cells from hydrogen peroxide damage These GTE polysaccharides suppressed the intracellular levels of reactive oxygen species ROS , as well as elevating antioxidative enzymes including superoxide dismutase SOD , catalase CAT , glutathione peroxidase GPx and glutathione GSH.
In conclusion, these studies suggesting GTE could modulate ocular neovascularization through multiple pathways.
Retinitis pigmentosa RP is a group of heterogenous retinal degeneration diseases caused by various gene mutations that would lead to progression loss of photoceptors. More than 50 genes have been found to be involved in RP One of the widely used animal models, P23H rats, recapitulate the slow rod photoreceptor degeneration in human RP A recent study reported that oral EGCG could help preserve the visual functions in the P23H rats Visual acuity and b wave ERG amplitudes, but not a wave ERG amplitudes, were significantly higher in the EGCG treated P23H rats, compared to the sham treatment group.
Interestingly, total antioxidant capacity TAC was significantly higher in the EGCG fed P23H rats compared to the sham group.
This study demonstrated potential benefits of EGCG in the RP animal model. Diabetic retinopathy DR is a diabetes mellitus DM associated irreversible blinding disease that would lead to chronic and progressive changes in the retinal microvasculature.
Hyperglycemia in the retinal Müller cells could alter the retinal microvasculature and enhance retinal neuron apoptosis EGCG was reported to induce autophagy, a physiological mechanism to remove cellular components, and protect cells from apoptosis cell death triggered by high glucose treatment in rat Müller cell primary culture In a cross-sectional community study in China, people who consumed tea for more than 20 years was associated with reduced odds of DR The consumption of green tea and non-green tea showed no statistical significance in the DR lower effects.
In addition, green tea was found to increase serum antioxidants and to lower the risk of developing type 2 DM 81 , In a cellular study, EGCG was found to protect human retinal pigment epithelial cells from pretreatment of methylglyoxal insults, major precursors of advanced glycation end products associated with to DM and DR These studies demonstrated the beneficial effects of GTE in protecting patients against DM and DR.
Glaucoma is a group of optic neuropathy with progressive retinal ganglion cell RGC loss and associated characteristic visual field defects Patients may present in a continuum of severity, ranging from initial asymptomatic stage to late symptomatic stage where there is significant visual impairment from visual field loss and eventually blindness While IOP was identified as the only modifiable risk factor for control of primary open angle glaucoma 86 , a certain group of glaucoma patients did not have elevated IOP throughout their course of disease, and the mechanism for normotension glaucoma is not completely clear.
In recent years, mounting evidence showed that neuroinflammatory processes, immune-relevant responses and oxidation play key roles in the pathogenesis of glaucoma 13 , A number of molecular pathways have been suggested to regulate inflammation in human and animal glaucoma models For examples, Toll-like receptor related pathway 87 , TNF-α pathway and a related protein FasL 88 , 89 , and the complement cascade 90 , 91 were involved in experimental glaucoma or in RGC death.
Besides, various pro- and anti-inflammatory cytokines such as interleukins ILs and interferons IFNs are suggested to involve in glaucoma during antigen presentation to T cells 15 , 92 , Although there were conflicting results, a meta-analysis suggested that flavonoids may have a role in improving visual function in patients with glaucoma and ocular hypertension Our recent study found that GTE could alleviate RGC degeneration in ischemic reperfusion rats Apoptosis, oxidative stress and inflammation were suppressed in RGC by the GTE treatment.
One major function of RGC, the pupillary light reflex, was also significantly rescued by GTE. This study suggested GTE could be developed as a novel treatment for glaucoma and other optic neuropathies.
In another mechanistic study, EGCG was found to stabilize the growth cone at the tip of growing Xenopus RGC by stabilizing F-actin within the growth cone These findings demonstrated EGCG could modulate RGC guidance, which could be further investigated its potential in glaucoma treatment.
In an experimental glaucoma mouse model, injection of microbeads in the anterior chamber was able to block the aqueous outflow and elevate IOP. The resulting RGC loss, but not IOP elevation, could be reversed by oral EGCG This study demonstrated EGCG could directly protect RGC, which may be developed as an alternative treatment to glaucoma in addition to the existing clinical practice of controlling elevated IOP in glaucoma patients.
Indeed, a randomized controlled study on the effect of short-term use of epigallocatechin-gallate EGCG , a powerful antioxidant, in ocular hypertension and open-angle glaucoma patients suggested that EGCG had a small but favorable effect on the inner retinal function as assessed by pattern electroretinogram in eyes with early to moderately advanced glaucomatous damages These experimental results suggest the beneficial effects of green tea catechins in glaucoma.
More large scale and long term studies are needed to evaluate the efficacy of green tea catechins in treating glaucoma.
Both infectious and autoimmune etiologies are involved in the inflammatory process on ocular surface. As one of the most common ophthalmic pathologies, dry eye disease affects millions of people in developed regions It has been recognized that dry eye is associated with inflammation of ocular surface, especially the Th1 and Th17 pathways.
Numerous inflammatory cytokines and chemokines such as IFN-γ, TNF-α, IL-1β, IL-6, IL, C-C motif ligand 2 CCL2 and matrix metalloproteinases MMPs have been implicated in dry eye — Several studies have suggested that green tea catechins, especially EGCG, which displays anti-inflammatory properties, are beneficial to the health of ocular surface.
Administration of the green tea catechins protected against autoimmune-induced pathological changes in the salivary glands in animal models suffering Sjögren's syndrome and helped to inhibit dry eye disease-related inflammation Cellular studies also demonstrated that EGCG inhibited release of IL-6, IL-8, monocyte chemotactic protein-1 MCP-1 , granulocyte-macrophage colony-stimulating factor GM-CSF , and granulocyte colony-stimulating factor G-CSF in human corneal epithelial cells, implying a therapeutic role for ocular surface inflammatory conditions Moreover, a double-blind randomized controlled clinical trial with 60 patients of dry eye and Meibomian Gland Dysfunction MGD showed that GTE improved the clinical symptoms, tear breakup time TBUT , and the health of meibomian glands.
No side effect of the treatment was observed To study corneal ulcer, proinflammatory cytokine IL-1β is able to induced corneal collagen degradation In IL-1β treated three-dimensional 3D cultured human corneal fibroblast, EGCG treatment could suppress collagen degradation in a concentration-dependent manner EGCG was found to suppressed the conversion of exogenous plasminogen to plasmin induced by IL-1β, leading to the inactivation of pro-MMP1.
The lower matrix metalloproteinase activities resulted in less collagen degradation. This study highlighted the potential of EGCG is treating corneal ulcer. Some ocular inflammation can be caused by systemic inflammatory diseases including ankylosing spondylitis, Behçet disease, and Vogt—Koyanagi—Harada disease.
Therefore, green tea and catechins could help to treat ocular inflammation by resolving relevant systemic inflammatory diseases. Taking a view outside the eye, green tea catechins also possess anti-inflammatory, antioxidative, antiproliferative, and antibacterial, and antiviral properties by binding to the corresponding biological molecules and regulating a variety of enzyme activities and signal transduction pathways In , Dr.
Tsuneo Kada of National Institute of Genetics of Japan reported that bacterial mutagenicity could be suppressed by green tea brew This had led to subsequent studies to investigate the protective effects of GTE against infections. Later, the anti-oxidative effect of GTE was identified Physiologically, GTE possesses the anti-bacterial and anti-viral properties against foodborne pathogenic bacteria, dental caries bacteria, Helicobacter pylori , Methicillin-resistant Staphylococcus aureus MRSA , influenza virus, human papilloma virus, and herpes virus Green tea consumption has also shown protections against autoimmune diseases in experimental models.
The effects are suggested to be owing to its high content of polyphenols. EGCG is the most abundant molecule among all catechins. Studies in animals showed that green tea catechins or EGCG can resolve autoimmune disorders such as inflammatory bowel disease IBD , , rheumatoid arthritis RA — , multiple sclerosis , type I diabetes T1D , and Sjögren's syndrome , Animal studies in experimental autoimmune encephalomyelitis revealed that EGCG attenuates the autoimmune inflammation by suppressing the proliferation of T cells and the production of pro-inflammatory cytokines, decreasing Th1 and Th17 populations and increasing Tregs in lymph nodes, spleen and the central nervous system CNS For centuries green tea has been extensively consumed as a daily beverage in Asia-pacific region such as China, Japan and India , It has been regarded as a safe agent to human.
Although green tea as a beverage is not equal to GTE, many patient-based studies did not identify any serious adverse effects by using low to moderate doses of GTE or its most biologically potent polyphenol constituent, EGCG , , However, GTE could possibly be contaminated by toxic elements, heavy metals and pesticides Most of these adverse effects were hepatitis.
Serum alanine aminotransferase ALT and bilirubin levels were elevated , And these adverse effects could be resolved spontaneously following the termination of green tea consumption. Histological verification of the liver indicated inflammatory reactions, cholestasis, occasional steatosis and necrosis.
The adverse effects were probably associated with the intra-individual differences in the metabolism of green tea catechins. Excessive oxidative stress may also contribute to the adverse effects in the liver Laboratory studies of GTE in animals have also revealed toxicity under high doses usage.
Isbrucker et al. Hemorrhage in the stomach and intestine was observed. These data implied that high doses of EGCG could induce toxicity in the liver, kidney and intestine Study in mice by Lambert et al. A 5-fold increase of hepatic lipid peroxidation, 9. However, these adverse effects inducing doses are much higher than the regular dietary consumption of green tea and the minimal effective doses suggested by previous studies.
The oral bioavailability of green tea catechins in human is low The plasma concentrations of green tea catechins after ordinary amount of green tea consumption in human were times less than the concentrations in in vitro studies — Many environmental and gastrointestinal conditions including temperature, acidity and other biological enzymes have been reported to affect the stability of GTE , Nanotechnology has been one of the major research directions to improve the stability of GTE Encapsulating green tea catechins with nanoparticles including liposome and other liposomal-like structures phytosomes and niosomes have been reported to improve the antioxidant activity and chemical stability of EGCG Nanocarriers made of polysaccharides including chitosan, cyclodextrins and alginate could protect catechins from degradation under a range of temperatures and pH conditions Proteins including bovine serum albumin, gelatin and β-lactoglobulin could protect EGCG against oxidative degradations and lessen the bitter taste of EGCG In terms of safety concerns of encapsulated green tea catechins, no cytotoxic effects were observed in the positive surface charge chitosan at concentration rang of 0.
These studies suggested encapsulation could enhance the bioavailability of green tea catechins efficiently. Asian and Mediterranean diets consisted of difference herbal molecules are gradually being appreciated due to their health benefits, including protective effects against neurodegenerative and cardiovascular diseases Natural components that are extracted from diet have offered further insights to explore novel therapeutic strategies for challenging diseases such as intraocular inflammation.
GTE, one of the agents possessing potent anti-inflammatory property, is promising for prevention and treatment of intraocular inflammation. Recent epidemiological findings show that green tea consumption is able to decrease the risk of cognitive dysfunction , It is becoming clear that the potent anti-inflammatory effects of GTE on the eye involve both infectious and autoimmune pathogenesis.
For future perspective, from the studies of autoimmune uveitis, although EGCG is the most abundant constituent of GTE, the efficacy of GTE in treating EAU mice could not be fully replicated by EGCG Therefore, in the future, other green tea catechins and non-catechins molecules should also be studied individually and in combinations to find out the best formulae for treating autoimmune uveitis.
In addition, these formulae can also be studied in combination with steroids, which may allow us to achieve better treatment outcomes.
Human beings are sharing many evolutionarily conserved mechanisms with other species which could have been inherited during evolution.
However, the findings of these experimental models cannot be directly applied to human, due to our complicated physiological and cultural conditions, which cannot be observed in the animal models. Clinical investigations are still warranted for translational studies from bench to bedside.
Similarly, in the case of GTE, the efficiency and safety studies provide a novel strategy for inhibiting disease progression in intraocular inflammation, which we have discussed in this review.
Future studies should focus on patients. Clinical trials could be organized to clarify the optimum dose of GTE in human to achieve the maximum health benefits and minimum side effects. 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.
Durrani OM, Tehrani NN, Marr JE, Moradi P, Stavrou P, Murray PI. Degree, duration, and causes of visual loss in uveitis. Br J Ophthalmol. doi: PubMed Abstract CrossRef Full Text Google Scholar. Gritz DC, Wong IG. Incidence and prevalence of uveitis in Northern California; the Northern California epidemiology of uveitis study.
Guly CM, Forrester JV. Investigation and management of uveitis. Bloch-Michel E, Nussenblatt RB. International Uveitis Study Group recommendations for the evaluation of intraocular inflammatory disease.
Am J Ophthalmol. Wakefield D, Chang JH. Epidemiology of uveitis. Int Ophthalmol Clin. Yang MM, Lai TY, Luk FO, Pang CP. The roles of genetic factors in uveitis and their clinical significance.
Krishna U, Ajanaku D, Denniston AK, Gkika T. Uveitis: a sight-threatening disease which can impact all systems. Postgrad Med J. Valdes LM, Sobrin L. Uveitis therapy: the corticosteroid options. Couret C, Ducloyer JB, Touhami S, Angioi-Duprez K, Rougier MB, Labalette P, et al. J Fr Ophtalmol.
Thomas AS. Biologics for the treatment of noninfectious uveitis: current concepts and emerging therapeutics. Curr Opin Ophthalmol.
Whitcup SM, Nussenblatt RB. Treatment of autoimmune uveitis. Ann N Y Acad Sci. Larson T, Nussenblatt RB, Sen HN. Emerging drugs for uveitis. Expert Opin Emerg Drugs. Chen SD, Wang L, Zhang XL.
Neuroprotection in glaucoma: present and future. Chin Med J. Google Scholar. Soto I, Howell GR. The complex role of neuroinflammation in glaucoma. Cold Spring Harb Perspect Med. Williams PA, Marsh-Armstrong N, Howell GR, Lasker Lasker IRRF, Initiative on Astrocytes and Glaucomatous Neurodegeneration Participants.
Neuroinflammation in glaucoma: a new opportunity. Exp Eye Res. Li G, Luna C, Liton PB, Navarro I, Epstein DL, Gonzalez P.
Sustained stress response after oxidative stress in trabecular meshwork cells. Mol Vis. PubMed Abstract Google Scholar. Kolko M, DeCoster MA, de Turco EB, Bazan NG. Synergy by secretory phospholipase A2 and glutamate on inducing cell death and sustained arachidonic acid metabolic changes in primary cortical neuronal cultures.
J Biol Chem. Kawano T, Anrather J, Zhou P, Park L, Wang G, Frys KA, et al. Prostaglandin E2 EP1 receptors: downstream effectors of COX-2 neurotoxicity. Nat Med.
Ergorul C, Ray A, Huang W, Wang DY, Ben Y, Cantuti-Castelvetri I, et al. Hypoxia inducible factor-1alpha HIF-1alpha and some HIF-1 target genes are elevated in experimental glaucoma. J Mol Neurosci. Wei X, Cho KS, Thee EF, Jager MJ, Chen DF. Neuroinflammation and microglia in glaucoma: time for a paradigm shift.
J Neurosci Res. Sun D, Qu J, Jakobs TC. Reversible reactivity by optic nerve astrocytes. Ambati J, Atkinson JP, Gelfand BD. Immunology of age-related macular degeneration. Nat Rev Immunol.
De Falco S. Antiangiogenesis therapy: an update after the first decade. Korean J Intern Med. Group CR, Martin DF, Maguire MG, Ying GS, Grunwald JE, Fine SL, et al.
Ranibizumab and bevacizumab for neovascular age-related macular degeneration. N Engl J Med. Schmidt-Erfurth U, Kaiser PK, Korobelnik JF, Brown DM, Chong V, Nguyen QD, et al. Intravitreal aflibercept injection for neovascular age-related macular degeneration: ninety-six-week results of the VIEW studies.
Doyle SL, Campbell M, Ozaki E, Salomon RG, Mori A, Kenna PF, et al. NLRP3 has a protective role in age-related macular degeneration through the induction of IL by drusen components.
Anderson OA, Finkelstein A, Shima DT. A2E induces IL-1ss production in retinal pigment epithelial cells via the NLRP3 inflammasome. PLoS ONE. Edwards AO, Ritter 3rd R, Abel KJ, Manning A, Panhuysen C, Farrer LA. Complement factor H polymorphism and age-related macular degeneration.
Yates JR, Sepp T, Matharu BK, Khan JC, Thurlby DA, Shahid H, et al. Complement C3 variant and the risk of age-related macular degeneration. Dunkelberger JR, Song WC. Complement and its role in innate and adaptive immune responses.
Cell Res. Luo C, Zhao J, Madden A, Chen M, Xu H. Complement expression in retinal pigment epithelial cells is modulated by activated macrophages. Alexander P, Gibson J, Cree AJ, Ennis S, Lotery AJ.
Complement factor I and age-related macular degeneration. The definition and classification of dry eye disease: report of the Definition and Classification Subcommittee of the International Dry Eye WorkShop Ocul Surf.
Stapleton F, Alves M, Bunya VY, Jalbert I, Lekhanont K, Malet F, et al. TFOS DEWS II epidemiology report. Ayyildiz T, Sezgin FM.
The effect of ocular demodex colonization on schirmer test and OSDI scores in newly diagnosed dry eye patients. Eye Contact Lens. Roszkowska AM, Oliverio GW, Aragona E, Inferrera L, Severo AA, Alessandrello F, et al.
Ophthalmologic manifestations of primary sjogren's syndrome. Ghosh S, O'Hare F, Lamoureux E, Vajpayee RB, Crowston JG. Prevalence of signs and symptoms of ocular surface disease in individuals treated and not treated with glaucoma medication.
Clin Exp Ophthalmol. Pisella PJ, Lala E, Parier V, Brignole F, Baudouin C. Ames P, Galor A. Cyclosporine ophthalmic emulsions for the treatment of dry eye: a review of the clinical evidence. Clin Investig. Perez VL, Pflugfelder SC, Zhang S, Shojaei A, Haque R. Lifitegrast, a novel integrin antagonist for treatment of dry eye disease.
Hara Y. Tea catechins and their applications as supplements and pharmaceutics. Pharmacol Res. Connors SK, Chornokur G, Kumar NB. New insights into the mechanisms of green tea catechins in the chemoprevention of prostate cancer. Nutr Cancer. Dostal AM, Arikawa A, Espejo L, Bedell S, Kurzer MS, Stendell-Hollis NR.
Green tea extract and catechol-O-methyltransferase genotype modify the post-prandial serum insulin response in a randomised trial of overweight and obese post-menopausal women. J Hum Nutr Diet. Gianfredi V, Vannini S, Moretti M, Villarini M, Bragazzi NL, Izzotti A, et al. Sulforaphane and epigallocatechin gallate restore estrogen receptor expression by modulating epigenetic events in the breast cancer cell line MDA-MB a systematic review and meta-analysis.
J Nutrigenet Nutrigenomics. Masukawa Y, Matsui Y, Shimizu N, Kondou N, Endou H, Kuzukawa M, et al. Determination of green tea catechins in human plasma using liquid chromatography-electrospray ionization mass spectrometry.
J Chromatogr B Analyt Technol Biomed Life Sci. Namal Senanayake SPJ. Green tea extract: chemistry, antioxidant properties and food applications — a review.
J Func Foods. CrossRef Full Text Google Scholar. Xing L, Zhang H, Qi R, Tsao R, Mine Y. Recent advances in the understanding of the health benefits and molecular mechanisms associated with green tea polyphenols.
J Agric Food Chem. Chu KO, Chan KP, Wang CC, Chu CY, Li WY, Choy KW, et al. Green tea catechins and their oxidative protection in the rat eye.
Chu KO, Chan KP, Yang YP, Qin YJ, Li WY, Chan SO, et al. Effects of EGCG content in green tea extract on pharmacokinetics, oxidative status and expression of inflammatory and apoptotic genes in the rat ocular tissues. J Nutr Biochem. Chu KO, Wang CC, Chu CY, Choy KW, Pang CP, Rogers MS.
Uptake and distribution of catechins in fetal organs following in utero exposure in rats. Hum Reprod. Green tea has been touted for a number of health benefits, such as fighting heart disease and cancer, thanks to its high concentration of disease-fighting antioxidants called catechins.
Researchers say catechins are among a number of antioxidants, including vitamin C, vitamin E, lutein, and zeaxanthin, thought to help protect the delicate tissues of the eye from glaucoma and other eye diseases.
In the study, published in the Journal of Agricultural and Food Chemistry, researchers fed laboratory rats green tea extract and then analyzed their eye tissues.
The results showed that different parts of the eye absorbed varying amounts of catechins. The area with the highest concentration of catechins was the retina, which is the light-sensing tissue that lines the back of the eye.
The area with the least absorption of catechins was the cornea, which is the clear, outer layer of the eye. The study also showed that a measure of antioxidant activity lasted for up to 20 hours after the drinking green tea extract.
Researcher Kai On Chu of the department of ophthalmology and visual sciences at the Chinese University of Hong Kong and colleagues say that their findings suggest that drinking green tea could be protective of the eyes. Further studies, however, will be needed to confirm a protective effect in humans.
More than a cozy warm drink, green Green tea extract and eye health aand help extfact eye health. Healh may have known green tea is healthy. It is obviously better than soda, or beverages full of sugar. Many have touted it for its multitude of health benefits. But, did you know that green tea is also an excellent food for your eye health?Video
Natural Eye Floater Treatment - 4 Ways to Treat Eye Floaters Nootropic Ingredients for Brain Function the tez few years, there have been hea,th studies that have been released which suggest that drinking green Green tea extract and eye health may provide you with numerous health benefits. Green tea extract and eye health more and more research coming out each rGeen regarding Green tea extract and eye health benefits of green tea, is there any chance that this super drink may also have a positive impact on our eyesight? A new study thinks so! A recent report on green tea released by Biosyntrx Nutritional Biotechnology suggests that drinking green tea may help to improve your eye health and combat dry eyes. A Chinese study suggests that EGCG is able to protect retinal ganglion cells against oxidative-stress injury and may be used as a potential neuroprotective drug.
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