文献类型：期刊文献

中文题名：儿茶素对顺铂所致人胚肾细胞氧化损伤的影响

英文题名：Effect of catechin on cisplatininduced oxidative damage in human embryonic kidney cells

作者：王海[1,2];连燕娜[1,2];高丽萍[1,2];曲丽洁[1,2];张东平[1,2]

第一作者：王海

机构：[1]北京联合大学应用文理学院;[2]生物活性物质与功能食品北京市重点实验室

第一机构：北京联合大学应用文理学院

年份：2017

卷号：29

期号：1

起止页码：51-54

中文期刊名：癌变．畸变．突变

收录：CSTPCD;;CSCD:【CSCD_E2017_2018】；

基金：北京市自然科学基金资助项目(7163211)

语种：中文

中文关键词：儿茶素;顺铂;肾毒性;抗氧化

外文关键词：catechin ; cisplatin; nephrotoxicity; antioxidant

摘要：目的:研究儿茶素对顺铂(DDP)所致人胚肾细胞(HEK293)氧化损伤的影响并探讨其作用机制。方法:体外培养HEK293细胞,分为对照组、DDP组、儿茶素组、儿茶素(5、10、20 mg/L)+DDP组。MTT法检测儿茶素和DDP分别作用后的HEK293细胞存活率,以及儿茶素预处理对DDP所致细胞存活率下降的影响。黄嘌呤氧化酶法检测细胞超氧化物歧化酶(SOD)活力,硫代巴比妥酸法测定细胞内丙二醛(MDA)含量,二硫代二硝基苯甲酸法测定还原型谷胱甘肽(GSH)的含量。结果:与对照组比较,随着浓度的增加,DDP导致HEK293细胞存活率逐渐降低,儿茶素导致细胞存活率先增加后降低。儿茶素预处理后,对DDP(20 mg/L)所致细胞存活率的抑制作用未见明显减弱(P>0.05),但与DDP组相比,能显著抑制DDP听致细胞内MDA含量的升高以及SOD活力和GSH含量的下降(P<0.05)。结论:体外培养条件下,儿茶素预处理虽不能改变DDP对HEK293细胞存活率的影响,但可在一定程度上缓解DDP所致HEK293细胞的氧化损伤。
OBJECTIVE： To investigate the mechanism and effect of catechin on cisplatin （DDP）-induced oxidative damage in HEK293 cells. METHODS ： Survival HEK293 cells in vitro after their exposure to catechin or DDP was determined. In addition, the effect of catechin pretreatment on DDP-induced cell growth inhibition was determined by the MTT method. Superoxide dismutase （SOD） activity was examined by the xanthine oxidase method. Malondialdehyde （MDA） content was measured by the thiobarbituric acid method. Glutathione （GSH） content was determined by the nitrobenzoic acid method. RESULTS： Cell survival rate decreased gradually as the DDP concentrations increased. Pretreatment with catechin caused increased cell survival initially hut decreased gradually afterward. The initial increase was not significant （P〉0.05）. However, catechin treatment significantly increased the intracellular MDA content, but decreased the SOD activity and GSH level compared with that in the DDP control group （P〈0.05）. CONCLUSION： Although catechin pretreatment did not improve the survivaX rate of DDP-treated HEK293 cells, it alleviated the DDP- induced oxidative damage.