Akt通路与丙泊酚后处理大鼠的脑保护作用

Akt Pathway and Neuroprotection of Propofol Postconditioning in Rats

目的:观察丙泊酚后处理对局灶性脑缺血再灌注大鼠神经元凋亡的影响及其与PI3K-Akt信号转导通路的关系。方法:采用Longa法建立局灶性脑缺血再灌注模型。60只雄性SD大鼠随机分成4组,每组15只。假手术组(S组)、缺血再灌注组(I/R组)、缺血再灌注+丙泊酚后处理组(P组)、缺血再灌注+丙泊酚后处理+LY294002(LY组)。分别进行神经功能评分、脑梗死体积测定、TUNEL凋亡计数、western-blotting检测Akt与p-Akt的水平。结果:与I/R组比较,P组脑梗死体积减小,细胞凋亡减少,磷酸化Akt的表达增加。而这种保护作用会被PI3K-Akt信号通路阻断剂LY294002所抑制。结论:丙泊酚后处理抑制缺血再灌注所致的神经元细胞凋亡,这种保护作用由生存信号通路PI3K-Akt的活化所介导。

Objective： To investigate the antiapoptotic effect of propofol postconditioning on neuronal cells after focal cerebral ischemia in rats and its relationship with PI3K-Akt signaling pathway. Methods： Middle cerebral artery occlusion models were performed in SD rats. Sixty rats were randomly divided into 4 groups with 15 rats in each group which included S group, I/R group, P group and LY group. The neurological deficit score, cerebral infarct volume, apoptotie index with TUNEL staining, stain for paraffin sections, levels of Akt and p-Akt with western blotting were detected respectively. Results： Comparing with I/R group, propofol reduced the cerebral infarct volume, inhibited apoptotic index, and increased the phosphorylation of Akt in P group. Those effects were inhibited by LY294002. Conclusion： Propofol inhibits the neuron apoptosis after focal cerebral ischemia and reperfusion injury in rats. This protective effect is induced by the activation of PI3K-Akt signaling pathway.