没食子儿茶素没食子酸酯对Cr^(6+)诱导的Vero及786-0肾细胞凋亡的影响  

Effect of epigallocatechin-3-gallate on the apotosis of Vero and 786-0 renal cells stressed by chromium in vitro

作　　者：胡秀芳[1] 杨贤强[2] 

机构地区：[1]浙江大学生命科学院,浙江杭州310029 [2]浙江大学茶学系,浙江杭州310029

出　　处：《中国药理学与毒理学杂志》2003年第2期136-140,共5页Chinese Journal of Pharmacology and Toxicology

摘　　要：目的　探讨没食子儿茶素没食子酸酯(EGCG)对肾脏受活性氧应激损伤的保护作用。方法　以Cr6 +应激诱导Vero和 786 0肾细胞凋亡为实验模型 ,用吖啶橙染色、流式细胞仪检测和DNA凝胶电泳等方法研究了EGCG对两种肾细胞凋亡的影响。结果　Cr6 +浓度依赖地降低Vero和 786 0细胞存活率 ,IC50 分别为 9.8和 8.6mg·L- 1;其中 4 0 0mg·L- 1/2hCr6 +处理可诱导Vero和 786 0细胞凋亡。2 0～ 6 0mg·L- 1EGCG有效抑制Cr6 +引起的Vero活细胞数下降 ,且 4 0mg·L- 1EGCG显著抑制该细胞凋亡 ;但EGCG对 786 0细胞没有相应的保护作用 ,相反促进 786 0细胞凋亡。结论　EGCG对正常肾细胞的氧化应激损伤有保护作用 ,但对肿瘤细胞的氧化损伤没有保护作用。AIM This study was conducted to identify the protection of epigallocatechin 3 gallate(EGCG) against the renal damage by reactive oxygen species(ROS). METHODS Cr 6+ was used to induce apotosis of renal cells(Vero cells and 786 0 cells) in vitro. The effect of EGCG on apotosis was investigated by fluorescent staining, DNA electrophoresis and flow cytometry. RESULTS Cr 6+ decreased the viability of Vero and 786 0 cells in a concentration dependent manner, and the IC 50 was 9.8 and 8.6 mg·L -1 , respectively. Treatment with Cr 6+ 400 mg·L -1 for 2 h caused the apotosis of both Vero and 786 0 cells. EGCG 40 mg·L -1 markedly inhibited the apotosis of Vero cells, but no effect was seen on 786 0. CONCLUSION EGCG protected Vero cells from damage by ROS, but promoted the apotosis of 786 0 cells. The selective effect of EGCG on the apotosis of normal and tumor cells induced by chromium is valuable in clinic.

关 键 词：肾脏 活性氧 应激损伤 没食子儿茶素没食子酸酯 铬 VERO细胞 786-0细胞 细胞凋亡 

分 类 号：R285[医药卫生—中药学]