氧化应激对Vero细胞的损伤及EGCG的保护作用  

Damage of Oxidant-stress and Effect of Epigallocatechin-3-gallate on Vero Cells in Vitro

作　　者：胡秀芳[1] 柴立红[2] 陈集双[1] 杨贤强[3] 

机构地区：[1]浙江大学生命科学院 [2]浙江大学原子核农业科学研究所 [3]浙江大学茶学系,浙江杭州310029

出　　处：《茶叶科学》2003年第2期105-109,共5页Journal of Tea Science

摘　　要：研究了氧化应激对肾细胞-Vero细胞的损伤及EGCG的保护作用.用MTT、吖啶橙染色和DNA凝胶电泳等方法研究了H2O2和Cr6+应激对Vero细胞的损伤,及EGCG对凋亡细胞的保护作用及其机理.结果表明,H2O2和Cr6+剂量效应地抑制Vero细胞活性,IC50分别为175.6和9.8mg·L-1;其中50 mg·L-1 H2O2和400 mg·L-1/2h Cr6+可诱导Vero细胞凋亡.0～60 mg·L-1 EGCG有效抑制H2O2和Cr6+应激引起的细胞活性下降,且40 mg·L-1 EGCG显著抑制细胞凋亡.对于Cr6+所诱导的细胞凋亡,EGCG的保护作用与EDTA和Vc的协同作用效果相当,表明清除活性氧和络合金属离子都有助于减轻Cr6+应激损伤.可见,EGCG通过清除活性氧和络合离子有效地保护了肾细胞免受应激损伤,这对易遭受活性氧损伤的肾脏无疑具有一定的临床价值.This study was conducted to identify the protection of antioxidant——epigallocatechin-3-gallate(EGCG) to the renal damage by oxidant-stress. H2O2 and Cr6+ were used to induce apoptosis of renal cells-----Vero cells in vitro. With these models of cell apoptosis, the effect of EGCG on apoptosis was investigated through Staining and DNA electrophoresis. As the results, H2O2 and Cr6+ decreased the viability of Vero cells in a dose-dependent manner, and the IC50 was 175.6 and 9.8 mgL- respectively. Both 50 mgL-1 H2O2 and 400 mgL-/2h Cr6+ caused the apoptosis of Vero cells. 40 mgL- EGCG markedly inhibited the apoptosis of Vero cells, and the effect was the same as that of Vc and EDTA in combination, indicating the simultaneous effect of antioxidation and chelating. So, EGCG protected Vero cells from damage through both ROS scavenging and ion-chelating, and this kind of effect is valuable to kidney usually exposed to ROS in clinic.

关 键 词：氧化应激 VERO细胞 损伤 EGCG 保护作用 肾细胞 细胞活性 机理 活性氧 络合金属离子 铬 

分 类 号：R692[医药卫生—泌尿科学]