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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 effects of nitroglycerin on phosphorylation of Akt and Bad (ser136) during cerebral ischemia / reperfusion in rats. Methods Thirty-six healthy Sprague-Dawley rats were randomly divided into sham-operation group, ischemia-reperfusion group (control group) and nitroglycerin group. Apoptosis of neurons in CA1 region of hippocampus was detected by using tar violet staining and phosphorylation of Akt and Bad (ser136) was detected by immunoblotting. Results The apoptosis of neurons in hippocampal CA1 area of nitroglycerin group was significantly less than that of control group (P <0.05). The phosphorylation of Akt and Bad (ser136) in nitroglycerin group was significantly higher than that of control group (P <0.05). Conclusion Nitroglycerin can significantly reduce neuronal apoptosis in hippocampal CA1 area after cerebral ischemia and reperfusion, and significantly increase the phosphorylation of Akt and Bad (ser136), which plays a protective role on cerebral ischemia-reperfusion injury.