关键词: 促酰化蛋白, 急性心肌梗死, 细胞外信号调节激酶1/2

Abstract: Objective To investigate the effect of acylation-stimulating protein(Asp) gene on cardiac function in mice with acute myocardial infarction(MI). Methods C57BL/6 wild-type mice and Asp^-/- mice were divided into four groups(C57,Asp^-/-,C57+MI and Asp^-/-+MI) respectively. Twenty-four hours after ligation of the anterior descending coronary artery, heart B-ultrasound was performed to detect the cardiac function, and the fasting blood glucose and body weight of the mice were measured before thoracotomy sampling. Evans blue-TTC staining was used to observe the area of viable myocardium, ischemic myocardium and myocardial infarction. The expression of interleukin-8 (IL-8), endothelial nitric oxide synthase (eNOS) and blood lipid profile was determined by ELISA. The expression of extracellular signal-regulated protein kinase 1/2 (Erk1/2) and phosphorylated p-Erk1/2 protein was determined by Western blot. Results The fasting blood glucose and body weight of Asp^-/- control group and Asp^-/- myocardial infarction group were higher than those of wild-type group(P＜0.05). After myocardial infarction, the EF and FS of the mice in the Asp^-/- group were lower than those in the wild-type myocardial infarction group, and the LVEDd and LVESd were increased (P＜0.05). The ischemic area of Asp^-/- myocardial infarction group was significantly larger than that of wild-type myocardial infarction group(P＜0.05). Compared with C57+MI mice, IL-8 in Asp^-/- myocardial infarction mice was elevated. The eNOS of wild-type and Asp^-/- myocardial infarction mice were lower than those before operation. Erk1/2 and p-Erk1/2 in Asp^-/- myocardial infarction group were significantly weaker than those in wild-type myocardial infarction group. Conclusions Asp gene may improve mouse cardiac function, inhibit myocardial apoptosis, and reduce myocardial damage in mice.

Key words: acylation stimulating protein, myocardial infarction, Erk1/2