【摘要】 目的证明血必净注射液(XBJ)对大鼠缺血性脑损伤的神经保护作用部分是通过PI3K/Akt途径介导的。方法采用大脑中动脉闭塞(MCAO)方法制作Sprague-Dawley(SD)大鼠的缺血性脑损伤模型。选用5组大鼠,观察一定浓度(10ml/kg)的XBJ对脑缺血再灌注损伤的保护作用。采用渥曼青霉素(Wortmannin)(0.25mg/kg)检测XBJ的神经保护作用是否与PI3K/Akt信号通路的激活有关。检测24h后脑梗死体积、神经功能缺损评分、裂解caspase-3及p-Akt蛋白表达。结果 XBJ可明显增加大鼠24h后的p-Akt蛋白的表达,缩小脑梗死体积,裂解caspase-3,降低神经功能缺损评分。然而,Wortmannin在很大程度上逆转了XBJ的这些作用。结论 XBJ通过增加p-Akt蛋白的表达,减少梗死范围,降低神经功能缺损评分,减少caspase-3的裂解而发挥神经保护作用,其作用部分是通过激活PI3K/Akt信号通路实现的。更多还原

【Abstract】 Objective We aim to demonstrate that neuroprotection afforded by Xuebijing Injection(XBJ)in rat ischemic brain injury is partly mediated via PI3K/Akt pathway.Methods The ischemic brain injury in Sprague-Dawley(SD)rats was made by Middle Cerebral Artery Occlusion(MCAO).Five groups rats were used to investigate the neuroprotective effect of certain concentration(10 ml/kg)of XBJ.Wortmannin(0.25 mg/kg)was used to test whether the neuroprotective effect of XBJ was associated with activation of the PI3K/Akt signaling pathway.Cerebral infarct volume,neurological deficit scores,cleaved caspase-3 and the expression of p-Akt protein at 24 hwere detected.ResultsXBJ significantly increased the expression of p-Akt protein,reduced the cerebral infarct volume,cleaved caspase-3 and attenuated neurological deficit scores in rats at 24 h.However,wortmannin partially reversed these effects of XBJ dramatically.Conclusion XBJ exerted the neuroprotective effect by increasing the expression of p-Akt protein and decreasing infarct size,neurological deficit scores,cleaved caspase-3,which was achieved partly by activation of the PI3K/Akt signaling pathway.更多还原