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  • Title: Resveratrol protects against oxidative damage of retinal pigment epithelium cells by modulating SOD/MDA activity and activating Bcl-2 expression.
    Author: Yang Y, Wu ZZ, Cheng YL, Lin W, Qu C.
    Journal: Eur Rev Med Pharmacol Sci; 2019 Jan; 23(1):378-388. PubMed ID: 30657580.
    Abstract:
    OBJECTIVE: Age-related macular degeneration (AMD) is mainly characterized by dysfunction of retinal pigment epithelium (RPE) cells. This study aimed to investigate the protective effects of resveratrol on oxidative damaged RPE cells. MATERIALS AND METHODS: Human D407 cells were divided into normal control (NC), H2O2 treated (H2O2, treating with H2O2 at a final concentration of 200 mol/l) and resveratrol treatment groups (treating with resveratrol at a concentration of 12.5, 25, 50 and 100 mg/l). Malondialdehyde (MDA) and superoxide dismutase (SOD) activities were examined using enzyme-linked immunosorbent assay (ELISA). 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) and cell count kit-8 (CCK-8) were used to examine cell viability. Cell cycle phase distribution and apoptosis of D407 cells were evaluated using flow cytometry assay. B-cell lymphoma-2 (Bcl-2) and cleaved caspase 3 expression were detected using quantitative real-time PCR (qRT-PCR) and Western blot assay, respectively. RESULTS: Resveratrol significantly decreased inhibitive ratios of D407 cell growth compared to that of H2O2 group (p<0.05). Resveratrol significantly increased SOD activity compared to that of H2O2 group (p<0.05). Resveratrol significantly reduced MDA activity compared to that of H2O2 group (p<0.05). Resveratrol affected cell cycle phase distribution of D407 cells compared to that of H2O2 group (p<0.05). Resveratrol significantly decreased the early stage and late stage apoptosis rates compared to that of H2O2 group (p<0.05). Resveratrol significantly enhanced Bcl-2 levels and decreased cleaved caspase 3 levels compared to that of H2O2 group (p<0.05). CONCLUSIONS: Resveratrol protected against the oxidative damage of RPE cells by modulating SOD/MDA activity and activating Bcl-2 expression.
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