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目的:探讨薯蓣皂苷抗心肌缺血再灌损伤的分子机制。方法:RT-PCR方法测定心肌线粒体Mn-SOD活性、流式细胞术检测血浆CD62p,CD63表达百分率,ELISA法测定血浆的血小板活化因子(PAF)浓度。结果:与正常组对照,缺血再灌损伤组的Mn-SOD表达显著减少,CD62p、CD63和PAF表达增加,薯蓣皂苷能提高心肌线粒体的Mn-SOD表达,减少CD62p、CD63以及PAF的表达。结论:薯蓣皂苷抗心肌缺血再灌损伤可能涉及抗自由基、抗血小板活化的分子机制。
Objective: To investigate the molecular mechanism of diosgenin against myocardial ischemia reperfusion injury. Methods: The activity of Mn-SOD in myocardial mitochondria was determined by RT-PCR. The percentages of CD62p and CD63 in plasma were determined by flow cytometry. The plasma platelet activating factor (PAF) concentration was measured by ELISA. RESULTS: Compared with the normal group, the expression of Mn-SOD in the ischemia-reperfusion injury group was significantly reduced, and the expression of CD62p, CD63, and PAF was increased. Dioscin could increase the mitochondrial Mn-SOD expression and reduce the expression of CD62p, CD63, and PAF. Conclusion: Diosgenin anti-myocardial ischemia reperfusion injury may involve the molecular mechanism of anti-free radical and anti-platelet activation.