EGCG对高糖诱导的HK-2细胞氧化应激损伤的保护作用

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

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。

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 nu- clear accumulation of Nrt2 in association with downstream activation of Nrt2 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.