中文摘要：

目的：探讨表没食子儿茶素没食子酸酯（EGCG）是否能对长波紫外线（UVA）诱导的人角质形成细胞（HaCaT细胞）氧化损伤和凋亡起保护作用以及其可能的作用机制。方法：将HaCaT细胞分成空白组、EGCG组、UVA照射组以及UVA照射＋EGCG组。采用四甲基偶氮唑蓝（MTT）比色法检测细胞活性，筛选最佳药物浓度；检测细胞上清液中的超氧化物歧化酶（SOD）和谷胱甘肽过氧化物酶（GSH-Px活性以及丙二醛（MDA）含量变化；流式细胞仪检测细胞膜电位变化；末端转移酶介导的缺口末端标记（TUNEL）法检测不同组细胞凋亡率。结果：UVA照射组的SOD和GSH—Px明显下降、MDA相应上升，线粒体膜电位下降，凋亡率上升（P〈0．05）。EGCG处理的细胞UVA照射后其活性以及上清液中的SOD、GSH—Px活性相对于未加药UVA照射组明显增加，MDA相应下降；线粒体膜电位上升，细胞凋亡率明显下降（P〈0．05）。结论：EGCG可以减少UVA诱导HaCaT细胞氧化损伤和细胞凋亡，其机制可能与增强抗氧化成分活性和减少氧自由基有关。

英文摘要：

Objective： To investigate whether epigallocatethi-3-gallate（EGCG） can protect HaCaT cells against oxidative damage and apoptosis from UVA irradiation and its possible mechanisms. Methods： The cultured HaCaT cells were divided into the control, EGCG, UVA irradiated and UVA irradiated ＋ EGCG groups. HaCaT cells were treated by 10 J/cm^2 UVA irradiation. The viability of cell proliferation was detected by MTT method. The activity of superoxide dismutase（SOD）, glutathione peroxidase （GSH-Px）, and the level of malondialdehyde（MDA） were detected with colorimetric methods. The cell membrane potential changes were detected by flow cytometry. The apoptosis rates were detected by TUNEL assay. Results： Under UVA irradiation, HaCaT cell viability, the activities of SOD, GSH-Px in HaCaT cells and the cell membrane potential decreased, the content of MDA and the apoptosis was ascensive （P〈 0.05）. But in EGCG treated groups, HaCaT cell viability, the activities of SOD, GSH-Px and the cell membrane potential in HaCaT cells increased, the content of MDA and the apoptosis rate of EGCG treated groups also decreased （P〈0.05）. Conclusion： EGCG can relieve the oxidation cell damaged and apoptosis from UVA irradiation to HaCaT cells by strengthening antioxidation and decreasing oxygen radicals.