目的 初步研究注射用益气复脉（冻干）（YQFM）对大鼠急性心肌梗死的作用及机制。方法 构建冠状动脉左前降支永久性结扎导致的急性心肌梗死大鼠模型，使用随机数字法将模型成功大鼠分为模型组、卡托普利片（阳性药，3.67 mg/kg）组和YQFM低、中、高剂量（0.433、0.867、1.734 g/kg）组；假手术组进行胸腔切开术，不造模。每天给药1次，连续尾iv给药14 d。心电图检测大鼠的造模情况，超声心动检测大鼠左心室射血分数（LVEF）；酶联免疫吸附（ELISA）法检测各组大鼠血清肌钙蛋白（Tn）、肌酸激酶同工酶MB（CK-MB）和乳酸脱氢酶（LDH）水平；心脏组织切片HE和Masson染色观察心肌纤维化程度；免疫组化和Western blotting法检测细胞外调节蛋白激酶1/2（ERK1/2）磷酸化水平变化。结果 与假手术组比较，大鼠造模后心电图均显示ST段抬高，P波波幅异常，表明急性心肌梗死大鼠模型构建成功；与模型组比较，YQFM低、中、高剂量组和卡托普利片组的LVEF显著升高（P<0.01、0.001）；YQFM低、中、高剂量组和卡托普利片组血清Tn和LDH水平均显著降低（P<0.01、0.001）； YQFM中、高剂量组和卡托普利片组CK-MB水平显著降低（P<0.05、0.01）；YQFM明显抑制大鼠心肌纤维化，明显降低p-ERK1/2水平。结论 YQFM明显改善急性心肌梗死大鼠心功能，机制可能与抑制ERK1/2磷酸化、抑制心肌纤维化相关。

Objective To investigate the effect and mechanism of Yiqi Fumai Lyophilized Injection (YQFM) on acute myocardial infarction in rats. Methods Rat model of acute myocardial infarction caused by left anterior descending coronary artery permanent ligation was established. The model rats were divided into YQFM low, medium, and high dose (0.433, 0.867, 1.734 g/kg) group, captopril (3.67 mg/kg) group, and model group by random number method. The sham operation group received pleurotomy without modeling. The drug was given once a day for 14 days. The electrocardiogram was used to detect the modeling of rats, and the echocardiography was used to compare the changes of cardiac function before and after treatment in rats with acute myocardial infarction. ELISA was used to detect the changes of serum biomarkers of acute myocardial infarction including Tn, CK-MB and LDH. Degree of myocardial fibrosis were observed by HE and Masson staining of heart tissue sections, and activated state of extracellular regulatory protein kinase 1/2 (ERK1/2) were detected by immunohistochemistry and Western blotting. Results Compared with sham operation group, ST segment elevation and abnormal P wave amplitude were observed in electrocardiogram after modeling, indicating successful establishment of acute myocardial infarction rat model. Compared with model group, LVEF in YQFM low, medium, high-dose groups and captopril tablet group was significantly increased (P<0.01 and 0.001). The serum Tn and LDH levels in YQFM low, medium high-dose groups and captopril tablet groups were significantly decreased (P<0.01 and 0.001). The level of CK-MB in YQFM medium, high dose groups and captopril tablet group was significantly decreased (P<0.05 and 0.01). YQFM significantly inhibited myocardial fibrosis and decreased p-ERK1/2 level in rats. Conclusion YQFM significantly improved cardiac function in rats with acute myocardial infarction, and the mechanism may be related to inhibiting ERK1/2 phosphorylation and inhibiting myocardial fibrosis.

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