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目的观察20(R)-人参皂苷Rg_3对大鼠缺血再灌注后迟发性神经元损伤的保护作用并探讨其作用机制。方法将健康雄性SD大鼠随机分为:假手术组、模型组、20(R)-人参皂苷Rg_3组和尼莫地平组。采用线栓法复制SD大鼠大脑中动脉暂时性局部脑缺血再灌注模型(MCAO),于再灌注72 h后进行大鼠神经功能学评分,用脱氧核糖核酸末端转移酶介导的原位缺口末端标记法(TUNEL)检测神经细胞凋亡,用原位杂交技术检测鼠脑中Calpain和Caspase-3 mRNA的表达。结果缺血2 h再灌注72 h后,与模型组比较,20(R)-人参皂苷Rg_3可显著改善大鼠的行为障碍,显著减少神经细胞凋亡数,显著降低CalpainⅠ和Caspase-3 mRNA的表达,并呈剂量依赖性。结论 20(R)-人参皂苷Rg_3通过抑制Calpain和Caspase-3的表达对大鼠缺血再灌注后迟发性神经元损伤起保护作用。
Objective To observe the protective effect of 20 (R) - ginsenoside Rg 3 on delayed neuronal injury induced by ischemia / reperfusion in rats and its mechanism. Methods Healthy male Sprague-Dawley rats were randomly divided into sham operation group, model group, 20 (R) -ginsenoside Rg 3 group and nimodipine group. The middle cerebral artery transient middle cerebral ischemia-reperfusion model (MCAO) of SD rats was replicated by thread occlusion. Neurological function scores of rats were evaluated 72 h after reperfusion, Neuronal apoptosis was detected by nick end labeling (TUNEL), and the expressions of Calpain and Caspase-3 mRNA were detected by in situ hybridization. Results Compared with the model group, 20 (R) - ginsenoside Rg_3 could significantly improve the behavioral disorders, significantly reduce the number of apoptotic neurons and significantly decrease the expressions of Calpain Ⅰ and Caspase-3 mRNA Expressed in a dose-dependent manner. Conclusion 20 (R) -ginsenoside Rg 3 can protect the neurons from delayed neuronal injury after ischemia-reperfusion in rats by inhibiting the expression of Calpain and Caspase-3.