白藜芦醇
活力测定
细胞凋亡
丙二醛
化学
免疫印迹
超氧化物歧化酶
分子生物学
细胞周期
流式细胞术
视网膜色素上皮
MTT法
细胞
男科
药理学
氧化应激
生物化学
视网膜
生物
医学
基因
作者
Yang Yang,Wu Zz,Y L Cheng,W Lin,Qu Chen
出处
期刊:PubMed
[National Institutes of Health]
日期:2019-01-01
卷期号:23 (1): 378-388
被引量:39
标识
DOI:10.26355/eurrev_201901_16786
摘要
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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