缺血性脑损伤中硝酸甘油对神经元的保护及Akt信号通路的影响

Protection of nitroglycerine on neurons and effect on Akt signaling pathway during ischemic cerebral stroke in rats

目的探讨硝酸甘油(NG)对大鼠缺血性脑缺血再灌注中Akt和Bad(ser136)磷酸化的影响。方法36只健康SD(Sprague-Dawley)大鼠随机分为假手术组、缺血再灌注组(对照组)、硝酸甘油组。以大鼠四肢动脉结扎脑缺血模型为基础,应用焦油紫染色法检测海马CA1区神经元凋亡,采用免疫印迹检测Akt和Bad(ser136)的磷酸化。结果硝酸甘油组脑海马CA1区神经元凋亡显著少于对照组(P<0.05);硝酸甘油组Akt、Bad(ser136)的磷酸化显著高于对照组(P<0.05)。结论硝酸甘油能显著减轻脑缺血再灌注后脑海马CA1区神经元凋亡,明显提高Akt、Bad(ser136)的磷酸化水平,对脑缺血再灌注损伤起到保护作用。

Objective To investigate the effect of NG on the phosphorylation of Akt and Bad （ser136） during ischemic cerebral stroke in rats. Methods 36 Adult male SD（Sprague-Dawley） rats were randomly dividod into sham-operated group, ischemia-reperfusion group （ control group）, NG opener treatment group （ NG group）. Basing on the four-vessel occlusion models,neuron apoptosis in CA1 region of hippocampus was detected by cresyl violet staining, the phosphorylation of Akt and Bad（ser136） were detected by immunoblotting. Resuits The number of apoptotic neurons in NG group were significantly more than that of control group （P 〈0.05）. The phosphorylation of Akt and Bad（ser136） in NG group was significantly less than that in control group （P 〈 0.05）. Conclusion Nitric oxide donor NG has a protective effect on neuron in CA1 region of hippocampus following cerebral ischemia-reperfusion by significantly increasing the phosphorylation of Akt and Bad （ser136） and neuronal apoptosis.