间歇性低氧预处理对心肌缺血损伤大鼠的心肌保护作用及其可能机制

Myocardial protection of intermittent hypoxia preconditioning on rats with myocardial ischemic injury and its possible mechanism

目的探讨间歇性低氧预处理对心肌缺血损伤大鼠的心肌保护作用及其可能机制。方法选取45只SD雄性大鼠,随机均分为对照组、实验1组和实验2组。对照组实施假手术,实验1组采用垫扎球囊法构建心肌缺血损伤模型,实验2组在间歇性低氧模型构建完成后30 min,同法制作心肌缺血损伤模型。心肌缺血损伤模型建立后2 h,检测3组大鼠的血清肌酸激酶同工酶(CK-MB)、谷胱甘肽和丙二醛水平,以及心肌组织核因子E2相关因子2(Nrf2)蛋白的表达水平。结果实验1组的血清CK-MB和丙二醛水平高于对照组,血清谷胱甘肽水平及心肌组织Nrf2蛋白表达水平低于对照组(均P<0.05)。实验2组的血清CK-MB和丙二醛水平低于实验1组,血清谷胱甘肽水平及心肌组织Nrf2蛋白表达水平高于实验1组(均P<0.05)。结论间歇性低氧预处理对心肌缺血损伤大鼠具有一定的心肌保护作用,这一作用或与转录因子Nrf2表达水平上调有关。

Objective To explore the myocardial protection of intermittent hypoxia preconditioning on rats with myocardial ischemia injury and its possible mechanism.Methods Forty-five SD male rats were selected,and then were randomly and equally divided into control group,experimental group 1 and experimental group 2.Sham operation was conducted in the control group;myocardial ischemia injury model was constructed by padding and ligation with a balloon in the experimental group 1;myocardial ischemia injury model was constructed using the same method in the experimental group 2 at 30 minutes after modeling of intermittent hypoxia.At 2 h after constructing myocardial ischemia injury model,the serum creatine kinase MB isoenzyme(CK-MB),glutathione and malondialdehyde levels,as well as the expression level of myocardial nuclear factor erythroid-2-related factor 2(Nrf2) protein were detected in the rats of the three groups.Results Compared to the control group,the experimental group 1 obtained higher serum CK-MB and MDA levels,lower serum glutathione level and myocardial Nrf2 protein expression level(all P<0.05).The experimental group 2 yielded lower serum CK-MB and MDA levels,higher serum glutathione level and myocardial Nrf2 protein expression level in comparison with the experimental group 1(all P<0.05).Conclusion Intermittent hypoxia precondition can exert a certain myocardial protective effect on the rats with myocardial ischemia injury,and this effect may be related to up-regulation of transcription factors Nrf2 expression.