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目的:研究三七总皂苷对小鼠脑缺血再灌注后神经元凋亡及凋亡的线粒体途径相关蛋白细胞色素C(CytC),半胱氨酰天冬氨酸蛋白酶-9(caspase-9),caspase-3和磷酸化c-Jun氨基末端激酶(p-JNK1/2)表达的影响,探讨其抗脑缺血后神经元凋亡的机制。方法:C57BL/6小鼠随机分成假手术组、模型组、三七总皂苷组及依达拉奉组,连续给药4 d后结扎双侧颈总动脉造成脑缺血20 min,再灌注24,48 h,用Tunel法检测神经元凋亡,Western-blot法检测脑组织caspase-9,caspase-3,CytC和p-JNK1/2蛋白的表达。结果:脑缺血再灌注后24,48 h,模型组神经元凋亡率增加,脑组织CytC,caspase-9,caspase-3,p-JNK1/2蛋白表达均显著增强,与假手术组比较,差异具有统计学意义(P<0.01)。三七总皂苷组神经元凋亡率显著下降,脑组织CytC,caspase-9,caspase-3,p-JNK1/2蛋白表达均显著降低,与模型组比较,差异均具有统计学意义(P<0.05或P<0.01)。结论:三七总皂苷可抑制脑缺血再灌注后神经元凋亡,其机制可能与其抑制JNK信号转导蛋白激活、抑制线粒体凋亡途径有关。
Objective: To study the effects of Panax Notoginseng saponins on neuronal apoptosis and apoptosis after cerebral ischemia-reperfusion in mice. CytC, c-caspase-9 ), caspase-3 and phosphorylated c-Jun N-terminal kinase (p-JNK1 / 2), and to explore the mechanism of neuronal apoptosis after cerebral ischemia. Methods: C57BL / 6 mice were randomly divided into sham operation group, model group, total saponins of Panax notoginseng group and edaravone group. After continuous administration for 4 days, bilateral common carotid arteries were ligated for 20 min and reperfusion 24 , 48 h. The apoptosis of neurons was detected by Tunel method. The expressions of caspase-9, caspase-3, CytC and p-JNK1 / 2 proteins were detected by Western-blot. Results: At 24 and 48 h after cerebral ischemia-reperfusion, the apoptotic rate of neurons increased and the expressions of CytC, caspase-9, caspase-3 and p-JNK1 / 2 in brain tissue increased significantly , The difference was statistically significant (P <0.01). The apoptosis rate of neurons in the Panax notoginseng saponins group was significantly decreased, and the protein expressions of CytC, caspase-9, caspase-3 and p-JNK1 / 2 in the brain tissue were significantly lower than those in the model group (P < 0.05 or P <0.01). Conclusion: Panax notoginseng can inhibit neuronal apoptosis after cerebral ischemia / reperfusion, and its mechanism may be related to the inhibition of JNK signal transduction protein activation and mitochondrial apoptosis pathway.