Green tea catechins are potent anti-oxidants that ameliorate sodium iodate-induced retinal degeneration in rats

ABSTRACT Green tea extracts exhibit anti-oxidative and anti-inflammatory actions in different disease conditions. We hypothesized that green tea extract and its catechin constituents

ameliorate sodium iodate-induced retinal degeneration in rats by counteracting oxidative stress. In this study, adult Sprague-Dawley rats were intravenously injected with a single dose of

sodium iodate. Green tea extract (GTE; Theaphenon-E) or combinations of its catechin constituents, including (−)-epigallocatechin gallate (EGCG), were administered intra-gastrically before

injection. Live imaging analysis using confocal scanning laser ophthalmoscopy and spectral-domain optical coherence tomography showed a progressive increase of degenerating profile across

the retinal surface and decrease in thickness of outer nuclear layer (ONL) at Day-14 of post-injection. These lesions were significantly ameliorated by Theaphenon-E and catechin combinations

with EGCG. Catechins with exclusion of EGCG did not show obvious protective effect. Histological analyses confirmed that Theaphenon-E and catechins containing EGCG protect the retina by

reducing ONL disruption. Retinal protective effects were associated with reduced expression of superoxide dismutase, glutathione peroxidase and caspase-3 and suppression of

8-iso-Prostaglandin F2α generation in the retina. In summary, GTE and its catechin constituents are potent anti-oxidants that offer neuroprotection to the outer retinal degeneration after

sodium iodate insult, among which EGCG is the most active constituent. SIMILAR CONTENT BEING VIEWED BY OTHERS COMBINATION OF _LACTOBACILLUS FERMENTUM_ NS9 AND ARONIA ANTHOCYANIDIN EXTRACT

ALLEVIATES SODIUM IODATE-INDUCED RETINA DEGENERATION Article Open access 24 May 2023 HOP FLOWER EXTRACTS MITIGATE RETINAL GANGLION CELL DEGENERATION IN A GLAUCOMA MOUSE MODEL Article Open

access 10 December 2020 ORAL 8-AMINOGUANINE AGAINST AGE-RELATED RETINAL DEGENERATION Article Open access 26 May 2025 INTRODUCTION Age-related macular degeneration (AMD) is a leading cause of

irreversible visual impairment and blindness in most developed countries, affecting 50 million elderlies worldwide1,2. It is a progressive neurodegenerative disease affecting the macula and

resulting in a significant loss of central vision in advanced stages. Advanced stages of AMD can be classified into dry and wet forms, represented by their respective clinical hallmarks of

geographic atrophy and choroidal neovascularization3. In geographic atrophy, the pathological characteristics are atrophy of choriocapillaries, disruption of associated retinal pigment

epithelium (RPE) and derangement of underlying photoreceptors4. RPE plays a multitude of important biological roles in regeneration of bleached visual pigments, formation and maintenance of

interphotoreceptor matrix and Bruch membrane, selective transport of fluids and nutrients between photoreceptors and choriocapillaries and phagocytosis of photoreceptors5. Lipofuscin, the

residual bodies of phagolysosomes, accumulates within the cytoplasm of RPE cells along aging6. It induces oxidative stress in RPE cells since lipofuscin, when exposed to light and high

oxygen tension, initiates the production of reactive oxygen species (ROS)7. Clinically effective therapy is limited to neovascular AMD by repeated intravitreal injection of anti-vascular

endothelial growth factor (VEGF) agents. However, there is still no efficient regimen for early AMD and geographic atrophy. Green tea extract (GTE) has been extensively shown to be

anti-oxidative, anti-inflammatory and anti-angiogenic8 and has been proposed for treatment and prevention of cancers, cardiac diseases, obesity, diabetes and neurodegenerative diseases.

There are eight principal types of catechins identified from green tea. The major ones are (−)-epicatechin (EC), (−)-epigallocatechin (EGC), (−)-epicatechin gallate (ECG) and

(−)-epigallocatechin gallate (EGCG). Among them, EGCG is the most abundant and potent antioxidant9. _In vitro_, in a cell culture model, EGCG reduces UVB-induced apoptosis in ARPE19 cells

via oxidative stress and the JNK1/c-Jun pathway10. _In vivo_, in an animal model of light- and sodium nitroprusside-induced photoreceptor degeneration, EGCG protects photoreceptor cells from

degeneration11,12. Other forms, including (+)-catechin (C), (+)-gallocatechin (GC), (−)-catechin gallate (CG), (−)-gallocatechin gallate (GCG), are present only in small quantities. We

previously showed that sodium iodate is a retinotoxin which selectively damages RPE by oxidative stress and disrupts the photoreceptor layer13. Sodium iodate-induced retinal degeneration in

rats has been used as an animal model for drug/treatment testing, including stem cells and growth factors14,15,16. However, the treatment effects of GTE and its constituents have not been

studied. Here, we hypothesized that GTE and its catechin constituents ameliorate sodium iodate-induced retinal degeneration in rats by counteracting oxidative stress induced by sodium

iodate. To address this hypothesis, we determined the treatment effects of oral intake of GTE or combinations of catechins on progressive RPE and photoreceptor degeneration induced by sodium

iodate in rats, using live imaging techniques including confocal scanning laser ophthalmoscopy (cSLO) and spectral-domain optical coherence tomography (OCT). The biochemical and

histological effects of catechin treatments on the levels of oxidative stress markers were also evaluated. RESULTS LONGITUDINAL _IN VIVO_ IMAGING OF SODIUM IODATE-INDUCED RETINAL

DEGENERATION WITH GREEN TEA CATECHIN TREATMENTS Fundus examination by cSLO showed the typical appearance of the retinal vessels and the optic nerve head. No obvious change was visible in the

retina of control animals 14 days after saline injection (Fig. 1A). In contrast, dramatic damages were observed in the retinas 14 days after injection, characterized by the presence of

small dark blots, corresponding to degenerating profiles in the outer nuclear and cone and rod layer, throughout the whole retinal surface and the hyporeflection of retinal vessels in all

retinas examined in this group (Fig. 1B). Pre-treatment with Theaphenon E, catechins mixture with EGCG, or EGCG alone reduced dramatically the degenerating profiles in the retina, as

indicated by the number and distribution of the blots (Fig. 1D–F). Catechins without EGCG did not produce obvious reduction in these degenerating profiles (Fig. 1C). Quantitative analysis of

the degenerative profiles showed that the number of blots increased progressively from 7 days to 14 days after injection of sodium iodate. Treatment with Theaphenon E, catechins mixture

with EGCG or EGCG alone reduced significantly the number of dark blots on both 7 and 14 days after sodium iodate injection (_p_ < 0.05), when compared to the vehicle-treated group (Fig.

1G). No statistically significant difference was observed among these groups. However, the decrease in rats treated with catechins mixture without EGCG was not significant (_p_ > 0.05).

OCT images showed that, starting from day 7 after sodium iodate injection, the outer nuclear layer (ONL) thickness was substantially reduced (Fig. 2A–F). This thinning of ONL was

significantly reverted after treatment with Theaphenon E, catechins with EGCG, or EGCG alone (_p_ < 0.01, compared to the vehicle-treated group; Fig. 2G). The effects were maintained on

Day 14 after injection. Catechins mixture without EGCG did not show such protective effect to the ONL (_p_ > 0.05). HISTOLOGICAL ANALYSIS OF SODIUM IODATE-INDUCED RETINAL DEGENERATION

WITH GREEN TEA CATECHIN TREATMENTS To validate the _in vivo_ imaging results, degenerating profiles were measured in histological sections of the retina collected 14 days after sodium iodate

injection. In the retina of sodium iodate injected rats, obvious damages were found in the RPE, cone and rod layer and ONL, forming series of irregular foldings in the outer regions of the

retina (Fig. 3A,B). These damages were observed in all animals injected with sodium iodate and in all regions of the retina. Treatment with catechin mixture without EGCG did not produce any

detectable changes to the lesions (Fig. 3C). However, EGCG, catechin mixture with EGCG and the GTE Theaphenon E substantially reduced these retinal damages (Fig. 3D–F). This protective

effect was supported by quantitative analysis of the damages in the outer retinal regions. The percentages of folded retina (total retinal length exhibiting irregular ONL vs total retinal

length) in histological sections cutting across the optic disc were measured. More than 50% of the retinal folding was significantly reduced after pre-treatment with EGCG, catechin mixture

with EGCG or Theaphenon E (_p_ < 0.05). The protective effect is most potent for Theaphenon E (Fig. 3G). No obvious protection was observed in rats treated with catechin mixture without

EGCG. These findings confirmed the live imaging results obtained by cSLO and OCT, demonstrating a potent protective effect of GTE to retinal degeneration induced by sodium iodate. EGCG is

the most important constituent. CHANGES OF OXIDATIVE STRESS MARKERS The effects of catechin treatment on the expression of oxidative stress related genes superoxide dismutase (_Sod1_),

glutathione peroxidase (_Gpx3_) and caspase 3 (_Casp3_) was investigated in the retina 24 hours after sodium iodate injection. These genes were expressed at basal levels in the saline

controls, but their expressions were increased significantly after sodium iodate injection (Fig. 4A–C). The elevated levels of _Sod1_ and _Gpx3_ were suppressed significantly after treatment

with Theaphenon E, catechins with EGCG or EGCG (_p_ < 0.05), when compared to the vehicle-treated group, but was not obvious for catechin mixture without EGCG (_p_ > 0.05; Fig. 4A,C).

The expression level of _Casp3_ was reduced after treatment with Theaphenon E, EGCG or catechin mixture with or without ECGC (Fig. 4B), suggesting a potent anti-oxidative and anti-apoptotic

effect of catechins against sodium iodate induced retinal damages. The anti-oxidative properties of catechins were also investigated using 8-iso-prostanglandin F2α (8-iso-PGF2α) as an

oxidative stress index. In retinas treated with 40 mg/kg sodium iodate, the level of 8-iso-PGF2α was drastically increased for more than 10 folds in 24 hours (Fig. 5). Treatment with

Theaphenon E, EGCG or catechin mixture with EGCG significantly reduced the 8-iso-PGF2α level in the retina (_p_ < 0.05, when compared to the vehicle-treated control). However, no

significant reduction was observed after treatment with catechin mixture without EGCG (_p_ > 0.05). DISCUSSION We have investigated the effects of GTE and its catechin constituents on

retinal lesions generated by sodium iodate-induced oxidative stress in adult rat retina. Major findings include: i) _in vivo_ imaging using cSLO and SD-OCT shows that sodium iodate induces a

progressive and consistent damage to the retina; ii) histological examinations reveal a loss of RPE and disruption of cellular arrangement in the cone and rod layer and the outer nuclear

layer; iii) these damages are alleviated effectively by the GTE Theaphenon E and by its catechin constituents containing EGCG; iv) GTE and its catechin constituents suppress significantly

the increases in _Sod1_, _Gpx3_ and caspase 3 and reduce production of 8-iso-PGF2α after sodium iodate insult. These findings demonstrate a potent protective effect of Theaphenon E and its

constituent catechins in outer retinal degeneration caused by oxidative stress and suggest a therapeutic use of GTE in ocular diseases, such as AMD, that involves degeneration of RPE and

photoreceptor cells. Sodium iodate is a known toxin to induce selective RPE damage by oxidative stress and consequently retinal degeneration17,18. Sod1 is one of the major antioxidant

enzymes that play a crucial role in scavenging superoxide. Gpx3 is shown to remove free radicals and superoxides by means of glutathione19. In this study, we observed a significantly

elevated expression of the Sod1 and Gpx3 in the retina after sodium iodate injection, suggesting an increased utilization for scavenging reactive oxygen species during the insult. These

oxidative damages are ameliorated by the catechins, which contain ortho-hydroxyl group in the B-ring and galloyl moiety in the C-ring that react directly with superoxide and reduce formation

of H2O220. The anti-oxidative effect of catechins is further shown by measuring the level of 8-isoprostane, a marker of oxidative stress. This molecule is a well characterized member of the

F2-isoprostanes family, a group of stable PGF2α isomers derived from non-enzymatic oxidation of arachidonic acid independent of cyclooxygenase activity21. In the current study, the surge of

8-isoprostane level due to oxidative stress was dramatically decreased after treatment with GTE or its catechin constituents, giving direct evidences of potent anti-oxidative effects of

these compounds. Moreover, analyses of different combinations of catechin constituents showed that the anti-oxidative effects are drastically reduced if EGCG is excluded. Therefore, EGCG is

the most active constituent that contributes to the anti-oxidative activities of GTE. However, it remains to be determined if other catechin constituents exert more potent anti-oxidative

effects at concentrations higher than those used in this study. Previous reports have demonstrated that apoptosis plays a pivotal role in photoreceptor degeneration in sodium iodate-treated

animals and that GTE and catechins possess anti-apoptotic effects. This has been shown in rats with photoreceptor degeneration, in which the number of TUNEL-labeled nuclei was significantly

reduced in catechins-treated eyes than in untreated eyes12. Results in the current study also support the anti-apoptotic action of catechins, as caspase-3 is highly suppressed after GTE and

catechin treatments, likely caused by a reduction in anti-oxidative stress. The neuroprotective effects of GTE are partly contributed by the accessibility of various catechin constituents to

the ocular tissues. Our recent studies have shown that oral administration of GTE can reach the retinal tissue in sufficient amount to protect it from detrimental insult of oxidative

stress22,23. In our previous study, when another GTE, Sunphenon DCF-1, is orally administered at the dose of 550 mg/kg to the rats, various catechin constituents are detected in various

tissues and compartments of the eye and the peak concentrations are reached from 0.5 to 12.2 hr23. GC is predominant in vitreous humor, whereas EGC and EC are enriched in the retina. These

catechins are sustained at high levels in the retina. However, penetration level of EGCG is not particularly high23. In Theaphenon E, the amount of individual catechin constituents is higher

than those in Sunphenon DCF-1, especially EGCG, resulting in increased accumulation of catechins in various ocular tissues. A mixture of catechins in GTE, such as that in Theaphenon E, is

better than purified catechins, for example EGCG, because of synergic effects of various catechin constituents on anti-oxidation and bioavailability. A comparison of neuroprotective effects

in our live imaging studies and histological sections shows that Theaphenon E and combination of catechins with EGCG are more potent than EGCG alone, suggesting additional and synergistic

effects among major and minor constituents of catechins in GTE. It would be important to determine the optimal composition that generates the most potent protecting effect against oxidative

stress-induced retinal degeneration. In summary, the results from our _in vivo_ and _in vitro_ investigations show that oral intake of GTE or its catechin constituents attenuates sodium

iodate-induced retinal degeneration in rats by rescuing RPE loss and disruption of ONL through a suppression of oxidative stress. Our findings suggest that GTE and its catechin constituents

can serve as potent therapeutic agents to retinal degeneration and support the notion that daily consumption of GTE is beneficial to patients suffering from AMD and retinal dystrophies where

oxidative stress is implicated24. METHODS ANIMALS All rats were treated according to Guidelines of the Association for Research in Vision and Ophthalmology (ARVO) Statement on Use of

Animals in Ophthalmic and Vision Research. Experimental protocol in this study was approved by the Animal Experimentation Ethics Committee of the Chinese University of Hong Kong. Adult

Sprague-Dawley rats, weighing 200 g to 250 g, were obtained from the Laboratory Animal Service Center of the Chinese University of Hong Kong. Animals were housed in standard condition,

maintained at 22 ± 1 °C, 40 ± 10% humidity and with 12:12 hour dark-light cycle. Standard rodent chow and water were provided _ad libitum_. For each experimental group, 5 rats were used for

the experiments. SODIUM IODATE AND DRUG ADMINISTRATION Sodium iodate (Sigma-Aldrich, St. Louis, MO) was dissolved in sterile normal saline at a stock concentration of 4% (w/v). The rats were

anesthetized by intraperitoneal (i.p.) injection of ketamine (35 mg/kg; Ketaset; Fort Dodge Animal Health, Fort Dodge, IA) and xylazine (5 mg/kg; TranquiVed; Vedco, Inc., St. Joseph, MO).

Intravenous injection (i.v.) of 40 mg/kg sodium iodate was given via the tail vein. This dosage was shown to be optimal concentration that induces extensive outer retinal lesion throughout

the whole retinal surface without causing obvious toxic effects to other major organs13. The control group was the rats injected i.v. with the same volume of normal saline. The catechin

constituents EGCG, EC, GC, EGC (purchased from Chengdu Biopurity Phytochemical, China) and the GTE Theaphenon E (provided generously by Dr. Yukihiko Hara, Department of Environmental

Physiology, Shimane University Faculty of Medicine, Japan) were suspended in distilled water. To determine the most active components of GTE, we studied the neuroprotective effect of GTE and

its major constituents. The dosages of catechins tested were in accord to the proportion of each constituent in the GTE Theaphenon E (EGCG: 70.53%, EGC: 4.61%, EC: 3.88%, GC: 0.64%)23. The

dosages of catechins in the experimental groups are as follows: i) Theaphenon E - 550 mg/kg, which has been shown in our earlier study to be the optimal dose that produces potent

anti-inflammatory effects against acute uveitis in the rat without causing obvious toxic actions to major organs22, ii) EGCG - 387.8 mg/kg; iii) catechins mixture with EGCG - 438.0 mg/kg,

contains EGCG (387.8 mg/kg), GC (3.53 mg/kg), EGC (25.4 mg/kg) and EC (21.4 mg/kg); iv) catechins mixture without EGCG - 50.3 mg/kg, with GC (3.53 mg/kg), EGC (25.4 mg/kg) and EC (21.4 

mg/kg). The catechins were fed intragastrically twice at 12 hours and 1 hour before sodium iodate injection. Each experimental group and control group consisted of five animals. CONFOCAL

SCANNING LASER OPHTHALMOSCOPY AND SPECTRAL-DOMAIN OPTICAL COHERENCE TOMOGRAPHY cSLO and spectral-domain OCT (HRA-II; Heidelberg Engineering GmbH, Dossenheim, Germany) were used for _in vivo_

imaging of the retina of live rats. The procedures were as described in our earlier report13. In brief, an illuminating wavelength of 870 μm with a bandwidth of 50 μm was used as a

broadband light source. A dual-beam simultaneous imaging with an infrared cSLO provides a planar visualization of the retina. The scan rate of the cSLO was 16 frames per second with

eye-tracking activated. Fifteen images at the same retinal location at the same focal depth were captured. These images were averaged automatically by the built-in software to augment the

signal-to-noise ratio and simultaneously displayed on a computer screen25. The Spectralis OCT was modified according to the technical advice from the manufacturer for OCT imaging of rats.

Retinal photographs and OCT images could be simultaneously captured on the exact retinal locus, which ensures the high quality of OCT imaging. In each retina, 4 different square regions,

each from the superotemporal, inferotemporal, inferonasal and superonasal quadrant, around the optic nerve head were scanned separately by the volume scan protocol, which consists of 19

evenly distributed B scans (1024 A scans for each B scan) covering a 20° × 15° area of the retina26. The images were captured before (Baseline) and after sodium iodate injection (on Day 7

and 14). Prior to imaging, rats were anesthetized and pupils were dilated by topical 1% tropicamide. During imaging, media clarity was maintained with sterile saline to the cornea. The

number of blots, which correspond to the degenerating profiles in outer regions of the retina, was analyzed by Photoshop (11.0; Adobe Systems Incorporated, San Jose, CA)16. In each retina, 4

different square regions (400 μm × 400 μm) with clear visualization of the blots were analyzed before and after injection by a blinded observer. HISTOLOGICAL ASSESSMENT OF THE RETINA On

post-injection day 14, the rats were terminated with overdose of sodium pentobarbital (20%, W/V) and perfused with phosphate buffered saline (PBS) followed by 4% paraformaldehyde

(Sigma-Aldrich) in PBS at pH 7.4. Eyes were removed and further fixed in 10% formalin before paraffin embedding. Five micrometer sections of the eye were collected at the pupil-optic nerve

position. The sections were stained with Hematoxylin and Eosin and images were captured by a light microscope (DMRB; Leica, Germany) connected to a Spot digital camera (Diagnostic Instrument

Inc, USA). ASSAY FOR 8-ISO-PGF2Α IN RETINA The 8-Iso-PGF2α assay was based on our previously published protocol21. Briefly, on post-injection day 1, the rats were sacrificed with overdose

of sodium pentobarbital. The retinas were dissected and homogenized in ice-cold Folch solution. The homogenate was washed in 0.5 ml 0.9% sodium chloride to remove water-soluble compounds and

protein residues. After centrifugation, the organic layer was collected and dried under nitrogen. The organic residues of the tissues were hydrolyzed by potassium hydroxide (15%) for 30 min

at 37 °C. After acidification by hydrochloric acid to pH 3, 8-iso-PGF2α was extracted by C18 and silica Sep-Pak, derivatized with pentafluorobenzyl bromide (PFBB) and purified by thin layer

chromatography (TLC). The isoprostane residues were scraped out, extracted by ethyl acetate and derivatized by N,O-bis-(trimethylsilyl)-trifluoroacetamide (BSTFA), then dried and dissolved

in dodecane for GC-NCI-MS analysis. GENE EXPRESSION ANALYSIS Total RNA was isolated and extracted by TRIzol reagent (Invitrogen) followed by the RNeasy extraction kit according to the

manufacturer’s protocol (Qiagen, Germany). Equal amount of total RNA (2 μg) from each sample was reverse-transcribed using SuperScript III cDNA synthesis kit (Invitrogen). Expression of

oxidative stress-related genes was evaluated by the SYBR Green PCR (Roche) using the LightCycler real-time PCR instrument (Roche). Gene-specific primers for all tested genes were listed in

Table 1. Thermal cycling conditions included an initial denaturation step at 95 °C for 3 min followed by 45 cycles at 95 °C for 30 sec and an annealing temperature at 60 °C for 30 sec. All

samples were run in triplicate and each well contained 20 μl as final volume, including 1 μl of cDNA, 10 μM gene-specific primers and 2x SYBR Green I (Roche). _Gapdh_ was used as

housekeeping gene. Negative controls for gene expression were those without RNA in the reverse transcription reaction and without cDNA in the SYBR green PCR reaction. The mathematical method

described by Pfaffl was used to evaluate the relative expression as compared with _Gapdh_27. STATISTICAL ANALYSIS All data were analyzed by non-parametric tests, Mann-Whitney U-test and

Wilcoxon signed rank test, were used to compare the mean of each experimental group with that of negative control group. Data were expressed as mean ± standard error of the mean (SEM). All

analyses were performed using PASW Statistics 18 (SPSS Science, Chicago, IL) and _p_ < 0.05 was considered as statistical significance. ADDITIONAL INFORMATION HOW TO CITE THIS ARTICLE:

Yang, Y. _et al_. Green tea catechins are potent anti-oxidants that ameliorate sodium iodate-induced retinal degeneration in rats. _Sci. Rep._ 6, 29546; doi: 10.1038/srep29546 (2016).

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real-time RT-PCR. Nucleic Acids Res. 29, e45 (2001). Article  CAS  Google Scholar  Download references ACKNOWLEDGEMENTS We are grateful to Dr. Yukihiko Hara (Department of Environmental

Physiology, Shimane University Faculty of Medicine, Japan) who generously provided Theaphenon E for this study. This work was supported by the Health and Medical Research Fund (project

number: 12130791 to T.K.N. and project number: 12130811 to C.P.P.) and the Research Grant Council General Research Fund (Ref. No.: CUHK14113815 to S.O.C.), Hong Kong. AUTHOR INFORMATION

Author notes * Pang Chi Pui and Chan Sun On contributed equally to this work. AUTHORS AND AFFILIATIONS * Department of Ophthalmology & Visual Sciences, The Chinese University of Hong

Kong, Hong Kong Yaping Yang, Yong Jie Qin, Yolanda W. Y. Yip, Kwok Ping Chan, Kai On Chu, Wai Kit Chu, Tsz Kin Ng & Chi Pui Pang * Department of Ophthalmology, Eye and ENT Hospital of

Fudan University, Shanghai, China Yaping Yang * Department of Obstetrics & Gynaecology, The Chinese University of Hong Kong, Hong Kong Kai On Chu * School of Biomedical Sciences, Faculty

of Medicine, The Chinese University of Hong Kong, Hong Kong Sun On Chan Authors * Yaping Yang View author publications You can also search for this author inPubMed Google Scholar * Yong Jie

Qin View author publications You can also search for this author inPubMed Google Scholar * Yolanda W. Y. Yip View author publications You can also search for this author inPubMed Google

Scholar * Kwok Ping Chan View author publications You can also search for this author inPubMed Google Scholar * Kai On Chu View author publications You can also search for this author

inPubMed Google Scholar * Wai Kit Chu View author publications You can also search for this author inPubMed Google Scholar * Tsz Kin Ng View author publications You can also search for this

author inPubMed Google Scholar * Chi Pui Pang View author publications You can also search for this author inPubMed Google Scholar * Sun On Chan View author publications You can also search

for this author inPubMed Google Scholar CONTRIBUTIONS T.K.N., C.P.P. and S.O.C. designed research; Y.Y., Y.J.Q., Y.W.Y.Y., K.O.C. and K.P.C. performed research; Y.Y., K.O.C., W.K.C. and

S.O.C. analyzed data; C.P.P. and S.O.C. supervised project; Y.Y., T.K.N., C.P.P. and S.O.C. wrote the manuscript. ETHICS DECLARATIONS COMPETING INTERESTS The authors declare no competing

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ARTICLE CITE THIS ARTICLE Yang, Y., Qin, Y., Yip, Y. _et al._ Green tea catechins are potent anti-oxidants that ameliorate sodium iodate-induced retinal degeneration in rats. _Sci Rep_ 6,

29546 (2016). https://doi.org/10.1038/srep29546 Download citation * Received: 17 February 2016 * Accepted: 20 June 2016 * Published: 07 July 2016 * DOI: https://doi.org/10.1038/srep29546

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