中文摘要：

目的探讨益气活血中药（生脉注射液联合血塞通注射液）对心肌梗死大鼠心脏蛋白激酶C（protein kinase C,PKC）表达的影响。方法 SD大鼠随机分为模型组、假手术组、卡托普利组和益气活血组。结扎大鼠心脏左冠状动脉前降支建立心肌梗死模型（假手术组只穿线,不结扎）。模型组和假手术组给予生理盐水;卡托普利组给予卡托普利片4.39 mg/（kg·d）溶解灌胃;益气活血组给予生脉注射液3.51 m L/（kg·d）联合血塞通注射液17.54 mg/（kg·d）腹腔注射。治疗4周后取材,称重计算心脏质量指数;RT-PCR法检测左心室心肌组织PKC mRNA的表达;Western blot法检测PKC蛋白的表达。结果与假手术组比较,模型组心脏质量指数显著增加（P〈0.01）,PKC的mRNA和蛋白表达亦显著增加（P〈0.05或P〈0.01）;与模型组比较,益气活血组和卡托普利组心脏质量指数显著降低（P〈0.05）,同时PKC的mRNA和蛋白表达也显著降低（P〈0.05或P〈0.01）。结论益气活血药（生脉注射液联合血塞通注射液）可以改善心脏重构,其机制与抑制心肌梗死后心肌组织PKC的高表达有关。

英文摘要：

Objective To study effects of Yiqi Huoxue drugs （ combine Shengmai injection with Xuesaitong injection） on expression of protein kinase C（ PKC） in rats with myocardial infarction. Methods SD rats were randomly divided into model group, sham operation group, captopril group and Yiqi Huoxue group. Model rats of myocardial infarction were established by occlusion of the left anterior descending coronary artery （ the sham operation group without occlusion of the left anterior descending coronary artery）. Captopril 4. 39 mg/（kg＆#183;d） and distilled water （for the sham operation and model groups） were administered orally. Yiqi Huoxue drugs （ combine Shengmai injection 3. 51 mL/（ kg＆#183;d） with Xuesaitong injection 17. 54 mg/（kg＆#183;d） were administered intraperitoneally. The cardiac mass index was recorded after 4 weeks of treatment. The expressions of PKC mRNA of myocardium in left ventricular were detected by real-time fluorescent quantitative polymerase chain reaction. And the expressions of PKC protein were observed by Western blot. Results Compared to the sham operation group, the cardiac mass and the ex-pressions of PKC mRNA and protein index in the model group increased significantly （ P〈0. 05 or P〈0. 01）. Compared to the model group, the cardiac mass index and expressions of Cx43 mRNA and protein decreased significantly in Yiqi Huoxue group and captopril group （ P〈0. 05 or P〈0. 01 ）. Conclusion Yiqi Huoxue drugs （ combine Shengmai injection with Xuesaitong injection ） can improve cardiac remodeling after myocardial infarction, which may through the mechanism of its suppression effects of the high expression of PKC in myocardial tissue after myocardial infarction.