Abstract：Objective To study the role of survivin in myocardial infarction rat model and the molecular pathway involved. Methods Left anterior descending artery (LAD) ligation and survivin-knockout methods were used to establish Survivin+/+/sham, Survivin+/-/sham, Survivin+/+/MI and Survivin+/-/MI rat groups (each n=10). Magnetic resonance imaging (MRI) and electrocardiograph (ECG) were employed to measure left ventricular function indexes, including ejection fraction (EF), fractional shortening (FS) and cardiac output (CO). Masson’s Trichrome staining was utilized to stain rat heart tissue, and then the fibrosis plaque rate was calculated. Apoptosis of rat cardiomyocyte was tested by TUNEL staining; finally, quantitative real-time PCR and Western blot assay were used to detect mRNA and protein expression of survivin and IL-6 in the four rat groups respectively. Results The EF and FS values in Survivin+/-/sham group both increased as compared with those in Survivin+/+/sham group (P<0.05), and the values in Survivin+/-/MI group were both higher than those in Survivin+/+/MI group (P<0.05). No statistically significant difference was found in the CO values (P>0.05). TUNEL-positive cells as well as fibrosis plaque had not been detected by TUNEL and Masson’s Trichrome staining respectively in Survivin+/+/sham and Survivin+/-/sham groups; moreover, the apoptotic rate of cardiomyocytes and the fibrosis fraction rate were significantly lower in Survivin+/-/MI group than in Survivin+/+/MI group (both P<0.05). Survivin mRNA expression in Survivin+/-/sham group was less than that in Survivin+/+/sham group (P<0.05), and it was higher in Survivin+/-/MI group than in Survivin+/+/MI (P=0.04). IL-6mRNA expression was higher in Survivin+/-/sham group than in Survivin+/+/sham group (P=0.02), but it was lower in Survivin+/-/MI group than in Survivin+/+/MI group (P=0.01). Western blot assay indicated that protein expression of Survivin and IL-6 showed consistent results with mRNA expression. Conclusions Survivin plays a vital role in myocardial infarction rat model by regulating apoptosis. Survivin haplo-insufficiency may increase cardiac function of myocardial infarction rat model, but its molecular mechanism requires further studies.
邓士兵, 周忠泉, 马莎, 周琼, 李汉芝. Survivin在心肌梗塞小鼠模型中的作用及机制研究[J]. 实用预防医学, 2018, 25(1): 73-77.
DENG Shi-bing, ZHOU Zhong-quan, MA Sha, ZHOU Qiong, LI Han-zhi. Role of survivin in myocardial infarction rat model and its mechanism. , 2018, 25(1): 73-77.
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