表没食子儿茶素没食子酸酯对肾缺血再灌注损伤的保护作用

Protective Effect of Epigallocatechin Gallate on Ischemia-reperfusion Injury

关键词:  表没食子儿茶素没食子酸酯  肾缺血再灌注损伤  Wnt/-catenin/p53

Key words:  EGCG  renal ischemia reperfusion injury  Wnt/β-catenin/p53

摘要:

目的 探讨表没食子儿茶素没食子酸酯(epigallocatechin gallate，EGCG)对大鼠肾缺血再灌注损伤的作用及机制。方法 通过结扎左侧肾动脉45 min同时去除右肾，再灌注24 h构建大鼠肾缺血再灌注损伤模型。大鼠随机分为EGCG组，假手术组和缺血再灌注损伤(IRI)组。EGCG组于造模前45 min腹腔注射EGCG 10，20，40，80 mg·kg^-1。通过观察肾脏组织病理变化，检测大鼠肾脏Wnt、β-catenin、p53、p21丙二醛(MDA)、过氧化氢酶(CAT)、谷胱甘肽过氧化物酶(GPx)、超氧化物歧化酶(SOD)的表达，以及肾脏和血清白介素6(IL-6)、干扰素(inteferon gamma，IFN-γ)和肿瘤坏死因子(TNF-α)的表达，评估EGCG对肾缺血再灌注损伤的作用及机制。结果 EGCG可改变肾组织病理，减轻肾脏损伤以及Wnt、β-catenin、p53、p21、MDA、IL-6、IFN-γ和TNF-α表达，增加CAT、GPX和SOD表达。结论 EGCG预处理可减轻肾缺血再灌注损伤，其作用机制与抑制Wnt/β-catenin/p53介导的炎症反应和氧化应激相关。

Abstract:

OBJECTIVE To investigate potential protection and mechanism of EGCG on kidney ischemia reperfusion injury. METHODS The model of renal ischemia reperfusion injury was induced by clamping the left renal artery for 45 min and reperfusion for 24 h with removing right kindey in rats. The EGCG group were pretreated with 10, 20, 40, 80 mg·kg^-1 EGCG at 45 min by intraperitoneal injection before modle. The pathlogical change of kidney tissues, the expression of Wnt, β-catenin, p53, p21, MDA, CAT, GPX, SOD, IL-6, IFN-γ and TNF-α were examined in rats to evalute the effect of EGCG in renal ischemia reperfusion injury. RESULTS EGCG can significantly decrease renal injury, pathlogical change and the expression of Wnt, β-catenin, MDA, IL-6, IFN-γ and TNF-α with increasing the expression of CAT, GPX and SOD. CONCLUSION EGCG can protect rats against kidney ischemia-reperfusion injury which is associated with suppressing Wnt/β-catenin/p53 signal pathway mediating inflammation and oxidative stress.