中文摘要：

目的探讨龙牙楤木总皂苷抗心肌缺血机制,为其应用于冠心病的防治提供理论基础。方法大鼠随机分为对照组（0.9%氯化钠溶液10 mL/kg）、龙牙楤木组（龙牙楤木总皂苷溶液0.5 g/kg）、氯吡格雷组（氯吡格雷溶液5 mg/kg）。连续灌胃5 d后,结扎前降支,缺血45 min,再灌注5 min。观察各组心肌组织病理改变程度,免疫组化法检测心内膜CD40L表达,并检测心肌丙二醛（MDA）及谷胱甘肽过氧化物酶（GSH-PX）水平。结果与对照组比较,龙牙楤木总皂苷组及氯吡格雷组可减少CD40L表达（P〈0.05）,提高心肌组织GSH-PX活力（P〈0.05）,但无统计学差异（P〉0.05）;龙牙楤木总皂苷组并可降低心肌MDA水平（P〈0.05）。结论龙牙楤木总皂苷可减轻心肌缺血再灌注CD40L表达,提高心肌GSH-PX活力,减少心肌MDA含量。

英文摘要：

Objective To investigate the mechanism of aralosides in antagonism of myocardial ischemia, and provide a theoretical base for it used for preventing and treating coronary heart disease （CHD）. Methods All rats were randomly divided into the control group （0.9% sodium chloride solution, 10 mL/kg）, aralosides group （aralosides solution, 0.5 g/kg） and clopidogrel group （clopidogrel solution, 5 mg/kg）. After intragastrical administration of drugs for 5 days respectively in all groups, the anterior descending coronary was ligated to induce ischemia for 45 minutes and then reperfused for 5 minutes. The pathological changes of myocardial tissue were observed in all groups, the expression of endocardial CD40L was detected by using immunohistochemistry, and levels of myocardial malondialdehyde （MDA） and glutathione peroxidase （GSH-PX） were detected. Results Compared with the control group, the expression of CD40L decreased （P 〈 0.05 ）, and vigour of myocardial GSH-PX increased （P 〈 0.05 ） in aralosides group and clopidogrel group, but the difference was not significant statistically （ P 〉 0.05 ）. The level of myocardial MDA decreased in the aralosides group （P 〈 0.05 ）. Conclusion Aralosides can decrease the expression of CD40L, improve the vigour of myocardial GSH-PX and reduce the level of myocardial MDA in rats with myocardial ischemia and reperfusion.