参麦注射液预先给药对心肌缺血-再灌注损伤大鼠心肌HMGB-1表达的作用

Effects of pre-injection Shenmai on cardiac HMGB-1 in myocardial ischemia-reperfusion injury rats

目的研究参麦注射液对心肌缺血-再灌注损伤大鼠心肌组织高迁移率族蛋白B1(HMGB-1)表达的作用。方法取30只SD大鼠随机均分为假手术组(Sham组)、心肌缺血-再灌注未干预组(IR组)、参麦注射液组(SM组),SM组每天腹腔内注射参麦注射液10ml/kg,连续3d,Sham组及IR组则按同样方法注射等容量生理盐水。Sham组分离左冠状动脉前降支,穿线后不结扎;IR及SM组开胸结扎左冠状动脉前降支,造成心肌缺血,30min后放松再灌注60min,建立心肌缺血-再灌注模型。ELISA法检测心肌组织HMGB-1的表达。显微镜下观察缺血心肌超微结构变化。结果与Sham组比较,IR组和SM组大鼠心肌组织HMGB-1含量明显增高(P<0.01)。与IR组相比,SM组大鼠心肌组织HMGB-1含量显著降低(P<0.01)。IR组心肌超微结构明显受损,SM组受损较轻。结论参麦注射液可降低缺血-再灌注损伤后大鼠心肌组织HMGB-1的表达水平,抑制炎症反应,减轻心肌缺血-再灌注损伤,保护心肌。这种作用可能与参麦注射液对炎症介质HMGB-1的基因表达和胞外释放具有明显抑制作用有关。

Objective To investigate the effect of Shenmai injection on cardiac high mobility group boxl （HMGB-1） in myocardial ischemia-reperfusion injury rats. Methods Thirty heathy male SD rats were randomly divided into three groups（n： 10, each）： Sham-operation（group Sham）, ischemia and reperfusion （group IR）, and Shenmai injection treatment （group SM）, then 10 ml/kg Shenmai injection were given in group SM and the 0. 9% NaC1 10 ml/kg were given in groups Sham and IR group for three days. After thoracotomy and ligation, the rats were injured by ischemia and relaxed 30 minutes later, then reperfusioned for 60 minutes, the myocardial ischemia-reperfusion models in rats were established during the experiment. The expressions of HMGB-1 was evaluated by ELISA. The myocardial samples were obtained for ultrastructure observation. Results Compared with group Sham, the expression level of HMGPrl in groups IR and SM were increased significantly （P〈0.01）. Compared with group IR, the expression level of HMGB-1 from myocardial in group SM were decreased significantly （P〈0.01）. Microscopic examination showed that myocardial ultrastructure in group SM was more slightly damaged than that in group IR. Conclusion These data suggest that： The expressions of HMGB-1 were increased significantly in ischemia-reperfused myocardial （MIR） rats. Shenmai injection can greatly depressed expression of HMGB-1. Shenmai injection may reduce systemic inflammatory response and protect myocardium ischemia/reperfusion injury. Inhibitory of HMGB-1 release may be the possible therapeutic mechanisms.