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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。
Objective To investigate the anti-ischemic mechanism of total saponins of Aralia elata, providing the theoretical basis for the prevention and treatment of coronary heart disease. Methods Rats were randomly divided into control group (0.9% sodium chloride solution 10 mL / kg), Aralia elata (0.5 g / kg total saponin solution), clopidogrel group (clopidogrel solution 5 mg / kg). After continuous gavage for 5 days, the descending branch was ligated, the ischemia was 45 min and the reperfusion was continued for 5 min. The degree of myocardial pathological changes in each group was observed. The expression of CD40L in endocardium was detected by immunohistochemistry. The level of malondialdehyde (MDA) and glutathione peroxidase (GSH-PX) in myocardium were measured. Results Compared with the control group, the total saponin of Aralia elata and clopidogrel group could reduce the expression of CD40L (P <0.05) and increase the activity of GSH-PX (P <0.05), but there was no significant difference (P> 0.05 ); Aralia elata total saponin group and can reduce myocardial MDA levels (P <0.05). Conclusion Aralia elata total saponin can reduce myocardial ischemia-reperfusion CD40L expression, increase myocardial GSH-PX activity, reduce myocardial MDA content.