眼针对脑缺血再灌注损伤大鼠PI3K/Akt通路影响的实验研究

摘要

目的 通过观察眼针治疗对磷脂酰肌醇-3-激酶(PI3K)/蛋白激酶B(Akt)通路的调控作用,探寻眼针治疗缺血性脑血管病的机制.方法 将64只SPF级Wistar大鼠分为空白组、假手术组、模型组(3h、24 h、72 h)、眼针组(3h、24 h、72 h).采用改良线栓法制备脑缺血再灌注损伤大鼠模型,通过眼针刺激对脑缺血再灌注损伤大鼠模型进行干预.观察眼针干预后大鼠神经功能缺损程度评分,并对各组大鼠缺血侧大脑皮层PI3K、Akt蛋白表达水平进行检测.结果 与空白组及假手术组比,模型组与眼针组大鼠出现不同程度的神经功能缺损;与模型组比眼针组24 h,72 h大鼠神经功能评分显著下降(P＜0.05);与空白组及假手术组比,模型组与眼针组各时间点PI3K、Akt蛋白表达增加,其中眼针组与模型组各时间点比增加更显著(P＜0.05).结论 眼针治疗能够激活PI3K、Akt信号通路,促进Akt磷酸化,发挥神经保护作用.%Objective:To explore the mechanism of eye acupuncture on cerebral ischemia-reperfusion rats by observing its effects on PI3K/Akt signaling path.Methods:62 SPF grade Wistar rats were divided into 8 groups:the blank group,Sham operation group,the model groups with 3 h,24 h and 72 h,the eye acupuncture groups with 3 h,24 h and 72 h.Improved suture-occluded method was adopted to establish cerebral ischemia-reperfu sion model,and eye acupuncture was applied to observe nerve function defect score and to detect the level of PI3K,Akt protein expression in ischemic cOrtex of rats in specific time point.Results:Compared with the blank group and sham operation group,model groups and eye acupuncture groups had different degrees of nerve function defect.Compared with the model group,nerve function defect score of the eye acupuncture 24 h and 72 h groups decreased obviously (P＜ 0.05).Compared with the blank group and sham opration group,the level of PI3K and Akt p53 protein expression of model groups and eye acupuncture groups increased.Compared with the model group,the expressions of PI3K and AK of eye acupuncture group also markedly increased at each point(P＜ 0.05).Conclusion:Eye acupuncture has neuro-protective effect on cerebral ischemia-reperfusion injury through the activation of PI3K/Akt signaling pathway and can promote the phosphorylation of Akt.