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Tsz Kin Ng, Jian Xiong Wang, Yaping Yang, Kai On Chu, Chi Pui Pang; Green tea extract restores oxidative stress-induced retinal pigment epithelial cell degeneration. Invest. Ophthalmol. Vis. Sci. 2015;56(7 ):2374.
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Oxidative stress is the most critical risk factor for retinal pigment epithelium (RPE) degeneration in age-related macular degeneration (AMD). Current AMD treatments only focus on relieving the symptoms, such as choroidal neovascularization, rather than controlling the disease origin. Green tea extract (GTE) has been shown to be anti-oxidative in different disease models. Here, we hypothesized that GTE could protect the oxidative stress-induced RPE degeneration. This study aims to determine the protective effect of GTE against the sodium iodate-induced RPE degeneration.
Human RPE cell line, ARPE-19, was treated with sodium iodate (10 mM) and GTE (Theaphenon®E; 100 µg/ml) for 5 days. The cell viability was determined by the MTT assay. For animal experiment, Sprague-Dawley rats were intravenously injected with single dose of sodium iodate (40 mg/kg) and then fed intragastrically with GTE (550 mg/kg) for 2 weeks. Markers for RPE (RPE65), oxidative stress (8-OHdG), tight junction (ZO-1) and apoptosis (caspase-3) were analyzed by immunohistochemistry. The study protocol was approved by the Animal Experimentation Ethics Committee of the Chinese University of Hong Kong, which is in accordance with the guidelines of the ARVO Statement for the Use of Animals in Ophthalmic and Vision Research.
Oxidative stress was induced by sodium iodate as confirmed by the nuclear signal of 8-OHdG. Moreover, the viability of sodium iodate-treated APRE-19 cells was reduced. For the sodium iodate-treated rats, photoreceptor rosettes were appeared along the whole retina. RPE65 and ZO-1 expressions were drastically reduced in RPE cells of sodium iodate-treated rats. In contrast, caspase-3 expression was increased in the outer segment of photoreceptor cells. In reverse, GTE rescued the cell death and oxidative stress in ARPE-19 cells as well as the disorganization of outer nuclear layer in rats. Furthermore, RPE65 and ZO-1 expressions in RPE were restored, whereas caspase-3 expression was reduced in the outer segment.
Sodium iodate induces oxidative stress, photoreceptor cell disorganization and apoptosis through RPE disintegration and dysfunction. GTE treatment restored RPE function and integrity as well as reduced photoreceptor cell death and disorganization. Our results demonstrated the therapeutic effect and the possible mechanism for GTE against sodium iodate-induced RPE changes.
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