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目的:探讨黄芪皂苷Ⅳ对大鼠心肌缺血/再灌注损伤的保护作用及抗凋亡作用。方法:研究黄芪皂苷Ⅳ对大鼠收缩压和舒张压的作用;建立大鼠心肌缺血/再灌注模型,在缺血前给予黄芪皂苷Ⅳ处理,观察心律失常的改变,测定血液中乳酸脱氢酶(LDH)、超氧化物歧化酶(SOD)和丙二醛(MDA)的变化,检测计算凋亡心肌细胞百分比及对P-STAT1、P-STAT3蛋白表达的调控作用。结果:黄芪皂苷Ⅳ可降低大鼠收缩压和舒张压,心肌缺血/再灌注前,预先给予黄芪皂苷Ⅳ有抗心律失常作用,降低血液中LDH和MDA含量,提高SOD活性,降低凋亡心肌细胞百分比,显著增加P-STAT1蛋白表达而同时降低P-STAT3蛋白表达。结论:黄芪皂苷Ⅳ对心肌缺血/再灌注损伤具有一定的保护作用,减少心肌细胞凋亡,其机制可能与抑制P-STAT1,诱导P-STAT3表达有关。
Objective: To investigate the protective effect of astragaloside Ⅳ on myocardial ischemia / reperfusion injury and its anti-apoptotic effect in rats. Methods: The effects of astragaloside IV on systolic and diastolic pressure in rats were studied. The rat model of myocardial ischemia / reperfusion was established. Astragaloside Ⅳ was administered before ischemia to observe the changes of arrhythmia. The levels of lactate dehydrogenase (LDH), superoxide dismutase (SOD) and malondialdehyde (MDA) were measured. The percentage of apoptotic cardiomyocytes and the regulation of P-STAT1 and P-STAT3 protein expression were detected. Results: Astragaloside Ⅳ could reduce the systolic and diastolic blood pressure in rats. Pretreatment with astragaloside IV had anti-arrhythmic effect, decreased the levels of LDH and MDA in the blood, increased the activity of SOD and decreased the apoptotic myocardium The percentage of cells significantly increased P-STAT1 protein expression while decreasing P-STAT3 protein expression. Conclusion: Astragaloside IV can protect myocardium from ischemia / reperfusion injury and decrease cardiomyocyte apoptosis. Its mechanism may be related to the inhibition of P-STAT1 and the induction of P-STAT3 expression.