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目的:比较普伐他汀、氟伐他汀和阿托伐他汀治疗新西兰兔心肌缺血再灌注损伤的疗效并探讨与疗效相关的机制。方法:实验分为普伐他汀、氟伐他汀和阿托伐他汀干预组,缺血再灌注前2 h经灌胃分别给予50 mg.kg-1的干预药物。术后2 h测量心肌梗死面积并检测缺血区内皮型一氧化氮合成酶活性。测定以上他汀类药物诱导血管内皮细胞表达内皮型一氧化氮合成酶的含量,并检测相关的p-Akt信号分子的表达。结果:在50 mg.kg-1剂量下,阿托伐他汀减少缺血再灌注后心肌梗死面积以及增加缺血区内皮型一氧化氮合成酶含量的作用较其它其它两种他汀类药物明显,差异有统计学意义(P<0.01)。阿托伐他汀诱导血管内皮细胞表达内皮型一氧化氮合成酶的作用较其它他汀类药物显著,差异有统计学意义(P<0.05),同时阿托伐他汀上调血管内皮细胞p-Akt蛋白的作用比其它两种他汀类药物更显著。结论:在相同剂量下,阿托伐他汀对于缺血再灌注损伤的疗效优于普伐他汀和氟伐他汀,机制可能为其具有更强的激活p-Akt信号通路并产生更多的具有保护性作用的内皮型一氧化氮合成酶的作用。
Objective: To compare the curative effect of pravastatin, fluvastatin and atorvastatin on myocardial ischemia-reperfusion injury in New Zealand rabbits and to explore the mechanism related to the curative effect. Methods: The experiment was divided into the intervention group of pravastatin, fluvastatin and atorvastatin, and the intervention group was given 50 mg.kg-1 respectively by gavage 2 h before ischemia-reperfusion. The area of myocardial infarction was measured 2 h after operation and the activity of endothelial nitric oxide synthase was detected in ischemic area. The above statin-induced expression of endothelial nitric oxide synthase was determined in vascular endothelial cells and the expression of the relevant p-Akt signaling molecule was examined. Results: Compared with the other two statins, atorvastatin reduced the area of myocardial infarction and the content of endothelial nitric oxide synthase in the ischemic area at 50 mg.kg-1, The difference was statistically significant (P <0.01). Atorvastatin induced endothelial cell expression of endothelial nitric oxide synthase than other statins, the difference was statistically significant (P <0.05), while atorvastatin increased vascular endothelial cell p-Akt protein The effect is more pronounced than the other two statins. Conclusions: Atorvastatin is more effective than pravastatin and fluvastatin on ischemia-reperfusion injury at the same dose, which may be attributed to the fact that atorvastatin has a stronger p-Akt signaling pathway and more protection Role of the role of endothelial nitric oxide synthase.