龙牙楤木总皂苷对大鼠心肌缺血再灌注损伤保护机制的研究

Study of protection mechanism of aralosides on myocardial ischemia/reperfusion injury in rats

目的:观察龙牙楤木总皂苷对缺血再灌注损伤心肌炎症因子ICAM-1表达及SOD的影响。方法:可逆性冠脉左前降支结扎缺血45min再灌注6h复制MI/R模型,Wistar雄性大鼠30只,随机分成模型组、龙牙楤木组、波立维组,每组10只。HE染色观察心肌病理学变化,测定心肌SOD活性,ELISA法测定血清sICAM-1的表达。结果:与模型组比较,龙牙楤木总皂苷、波立维均能显著降低缺血再灌注大鼠血清LDH含量,显著升高SOD的活性,缺血45min再灌注6h血清sICAM-1有明显表达,各组之间无统计学差异。结论:龙牙楤木总皂苷对MI/R有保护作用,可能是通过增加SOD的活力,对抗氧自由基对心肌细胞的毒害作用,减轻心肌细胞的损伤而实现的。

Objective： To investigate the effects of aralosides on expression of inflammatory molecule ICAM-1 and the activity of superoxide dismutase（SOD） in rats after myocardial ischemia/reperfusion（MI/R） injury.Methods： A model of myocardial ischemia 45min followed by 6h reperfusion was made by reversibly ligating coronary left descending artery.30 Wistar rats were divided randomly into 3 groups： ischemia reperfusion group,aralosides group,Plavix group.HE staining was used to observe the pathological changes of myocardic tissues.The activity of SOD was measured too.ELISA was used to determine sICAM-1 expression in myocardium.Results： In rats treated by aralosides or Plavix,the lactate dehydrogenase（LDH） activity was significantly decreased.Meamwhile,Aralosides and Plavix raised the activity of superoxide dismutase（SOD）.ICAM-1 expression was detected in myocardium after ischemia 45min followed by 6h reperfusion.In rats treated by aralosides or Plavix,ICAM-1 expression remained unchanged.Conclusion： Aralosides could protect myocardium from inflammatory injury during MI/R,which may be achieved by increasing the activity of SOD,confronting the toxic action of oxygen radical to cardiocytes and decreasing the injury of cardiocytes.