目的 初步研究注射用益氣復(fù)脈（凍干）（YQFM）對大鼠急性心肌梗死的作用及機(jī)制。方法 構(gòu)建冠狀動(dòng)脈左前降支永久性結(jié)扎導(dǎo)致的急性心肌梗死大鼠模型，使用隨機(jī)數(shù)字法將模型成功大鼠分為模型組、卡托普利片（陽性藥，3.67 mg/kg）組和YQFM低、中、高劑量（0.433、0.867、1.734 g/kg）組；假手術(shù)組進(jìn)行胸腔切開術(shù)，不造模。每天給藥1次，連續(xù)尾iv給藥14 d。心電圖檢測大鼠的造模情況，超聲心動(dòng)檢測大鼠左心室射血分?jǐn)?shù)（LVEF）；酶聯(lián)免疫吸附（ELISA）法檢測各組大鼠血清肌鈣蛋白（Tn）、肌酸激酶同工酶MB（CK-MB）和乳酸脫氫酶（LDH）水平；心臟組織切片HE和Masson染色觀察心肌纖維化程度；免疫組化和Western blotting法檢測細(xì)胞外調(diào)節(jié)蛋白激酶1/2（ERK1/2）磷酸化水平變化。結(jié)果 與假手術(shù)組比較，大鼠造模后心電圖均顯示ST段抬高，P波波幅異常，表明急性心肌梗死大鼠模型構(gòu)建成功；與模型組比較，YQFM低、中、高劑量組和卡托普利片組的LVEF顯著升高（P<0.01、0.001）；YQFM低、中、高劑量組和卡托普利片組血清Tn和LDH水平均顯著降低（P<0.01、0.001）； YQFM中、高劑量組和卡托普利片組CK-MB水平顯著降低（P<0.05、0.01）；YQFM明顯抑制大鼠心肌纖維化，明顯降低p-ERK1/2水平。結(jié)論 YQFM明顯改善急性心肌梗死大鼠心功能，機(jī)制可能與抑制ERK1/2磷酸化、抑制心肌纖維化相關(guān)。

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.

R285.5