天然产物研究与开发 ›› 2016, Vol. 28 ›› Issue (5): 673-679.doi: 10.16333/j.1001-6880.2016.5.006

• 研究论文 • 上一篇    下一篇

EGCG对高糖诱导的HK-2细胞氧化应激损伤的保护作用

代春美*,宋雨泽,杨伟,胡相卡,陈香   

  1. 辽宁医学院,锦州 121001
  • 出版日期:2016-05-28 发布日期:2016-09-06

EGCG Protects HK-2 Cells Damage Induced by High Glucose against Oxidative Stress

DAI Chun-mei*,SONG Yu-ze,YANG Wei,HU Xiang-ka,CHEN Xiang   

  1. Liaoning Medical University,Jinzhou 121001,China
  • Online:2016-05-28 Published:2016-09-06

摘要: 探究表没食子儿茶素没食子酸脂(EGCG)对高糖诱导的人肾小管上皮细胞HK-2氧化应激损伤的保护作用及其相关机制。用EGCG干预可以显著提高HK-2细胞抗氧化能力,抑制高糖诱导的细胞内ROS水平升高,提高细胞活力(P<0.05),并呈现剂量依赖效应。同时,研究发现EGCG能显著诱导HK-2细胞Nrf2核转位,并且其下游的Ⅱ相解毒酶HO-1蛋白表达水平也相应提高,Nrf2 mRNA的表达含量也相应升高(P<0.05)。说明EGCG可能通过激活Nrf2/ARE通路,发挥对高糖诱导的HK-2细胞氧化应激损伤的保护作用。

关键词: EGCG, 高糖, Nrf2/ARE信号通路, 氧化应激

Abstract: The aim of this study was to investigate the protective effect and mechanisms of epigallocatechin gallate(EGCG) against oxidative stress of HK-2 cells induced by high glucose.The results showed that EGCG intervention can improve the antioxidant capacity of HK-2 cells significantly,suppress the ROS levels in cells induced by high glucose,improve the cell vitality in a dose-dependent effect(P<0.05).Meanwhile,it was shown that EGCG can also cause nuclear accumulation of Nrf2 in association with downstream activation of Nrf2 mediated oxidative response genes such as HO-1,and the expression level of Nrf2 mRNA increased accordingly also(P<0.05).Hence,it was concluded that EGCG may protect against the oxidative damage of HK-2 cells induced by high glucose via the activation of Nrf2/ARE signal pathway.

Key words: EGCG, high glucose, Nrf2/ARE signal pathway, oxidative stress

中图分类号: 

R285.5