丙泊酚抑制脑缺血再灌注损伤大鼠细胞凋亡及其机制

摘要

目的 探讨丙泊酚对脑缺血再灌注损伤细胞凋亡的影响及其机制.方法 构建脑缺血再灌注损伤大鼠模型,同时设置假手术组,以用丙泊酚处理后的脑缺血再灌注大鼠模型为丙泊酚组,以脑缺血再灌注大鼠模型为对照组.对大鼠进行神经功能评分,取各组大鼠脑组织,氯化三苯基四氮唑(TTC)法检测脑梗死体积,脱氧核糖核苷酸末端转移酶介导的缺口末端标记法(TUNEL)检测细胞凋亡,Western blot检测活化的含半胱氨酸的天冬氨酸蛋白水解酶3(Cleaved Caspase-3)、蛋白激酶B(Akt)、磷酸化蛋白激酶B(p-Akt)表达水平.结果 假手术组细胞凋亡率、Cleaved Caspase-3水平均明显低于对照组,而p-Akt水平明显高于对照组(P<0.05).丙泊酚组神经功能评分、脑梗死体积、细胞凋亡率、Cleaved Caspase-3水平均明显低于对照组,而p-Akt水平明显高于丙泊酚组(P<0.05).结论 丙泊酚能够抑制脑缺血再灌注损伤导致的细胞凋亡,减轻脑缺血再灌注神经损伤,作用机制可能与Cleaved Caspase-3、p-Akt表达水平有关.%Objective To explore the effects of propofol on apoptosis and its mechanism of cerebral ischemia reperfusion injury in rats.Methods The rat model of cerebral ischemia reperfusion were established, and the sham operation group was set up.The rat model of cerebral ischemia reperfusion treated with propofol was used as propofol group, rat model of cerebral ischemia reperfusion was used as control group.Neurological function score were performed in rats.Brain tissue were acquired, TTC was used to detect cerebral infarction volume, TUNEL to detect apoptosis, Western blot to detect Cleaved Caspase-3, Akt, p-Akt expression level.Results The apoptosis rate and Cleaved Caspase-3 level in the sham operation group were significantly lower than those in the control group, the level of p-Akt was significantly higher than that of control group (P<0.05).The neurological function score, cerebral infarction volume, apoptosis rate and Cleaved Caspase-3 level in propofol group were significantly lower than those in control group, the level of p-Akt was significantly higher than that of propofol group (P<0.05).Conclusion Propofol can inhibit apoptosis induced by cerebral ischemia reperfusion injury, decrease cerebral ischemia reperfusion injury.The mechanism may be related to the expression level of Cleaved Caspase-3 and p-Akt.