染料木素磺酸钠激活ERK信号调节脑缺血凋亡相关基因的表达

GSS activating ERK signal to regulate the expression of apoptosis related genes in a rat with model of ischemic stroke

目的:初步探讨染料木素磺酸钠(genistein-3'-sodium sulfonate,GSS)是否通过ERK信号对大鼠脑缺血再灌注损伤诱导的凋亡起调控作用。方法:采用大鼠大脑中动脉栓塞(MCAO)动物模型,给予GSS处理后,Western blot方法测定皮层半暗带区脑组织p-ERK的蛋白表达情况。ERK抑制剂干预后,qPCR检测Bax、Bcl-2、Caspase 3的mRNA的表达情况。结果:①与对照组相比,模型组缺血半损伤区脑组织p-ERK的蛋白表达水平明显降低,经GSS治疗后p-ERK的蛋白表达水平显著升高。②与对照组相比,模型组缺血半损伤区脑组织Bax和Caspase 3的mRNA水平明显升高,Bcl-2的mRNA水平明显降低,经GSS治疗后,Bax和Caspase 3的mRNA水平显著下降,Bcl-2的mRNA水平显著升高。ERK抑制剂(U0126)阻断了GSS的作用。结论:染料木素磺酸钠可能通过ERK信号调节凋亡相关基因表达对脑缺血再灌注损伤大鼠起保护作用。

Objective:To investigate whether genistein-3'-sodium lignosulfonate(GSS)can regulate the apoptosis induced by cerebral ischemia-reperfusion injury in rats by ERK signal.Methods:The expression of p-ERK was measured by Western blot after GSS treatment in MCAO rats.The expression of Bax,Bcl-2 and caspase-3 mRNA was detected by qPCR.Results:①Compared with the control group,the protein expression level of p-ERK in the model group was significantly lower than that in the control group.②Compared with the control group,the mRNA level of Bax and Caspase-3 in the model group was significantly increased,and the mRNA level of Bcl-2 was significantly decreased.After GSS treatment,the mRNA level of Bax and caspase-3 was significantly decreased,and the mRNA level of Bcl-2 was significantly increased.ERK inhibitor(U0126)abolished the effect of GSS.Conclusions:Genistein sulfonate may play a protective role in rats with cerebral ischemia-reperfusion injury by regulating the expression of apoptosis related genes through ERK signal.