中国应用生理学杂志 ›› 2016, Vol. 32 ›› Issue (6): 514-518.doi: 10.13459/j.cnki.cjap.2016.06.007
Miao YU1, Zhi-hui HE1, Li-ying XUAN1, Xiao-tong SHAN1, Jie LONG1, Jing-yi FENG1, Yu WANG1, Ming ZHAO2
Miao YU1, Zhi-hui HE1, Li-ying XUAN1, Xiao-tong SHAN1, Jie LONG1, Jing-yi FENG1, Yu WANG1, Ming ZHAO2
摘要: Objective: To investigate the effect of creatine phosphate sodium (sodium phosphocreatine) on miRNA378, miRNA378* and calumenin mRNA in adriamycin-injured suckling mouse myocardium. Methods: The suckling mouse myocardium of primary culture were randomly divided into control group, adriamycin group and treatment group. To identify the suckling mouse myocardium, Smooth muscle actin-α (α-SMA) was monitored by immunohistochemical method. Cardiac function was evaluated by transthoracic echocardiography. The mRNA change of miRNA378, miRNA378* and calumenin mRNA were detected by quantitative real-time PCR. The expression of calumenin and GRP78 were identified by western blot. Results: Mitochondrial damage and vacuolization were found in adriamycin-induced suckling mouse myocardium compared with control group, while creatine phosphate sodium could reduce this phenomenon. Compared with the control group, the mRNA of miRNA378, miRNA378* and calumenin in adriamycin group was reduced, while creatine phosphate sodium could increase this phenomenon. The expression of calumenin and GRP78 were decreased after adriamycin treatment in suckling mouse myocardiums, creatine phosphate sodium increased the expression of calumenin and GRP78. Conclusion: The results of this experiment might be closely related to the effects of that creatine phosphate sodium reduced the pathological mechanism of suckling mouse myocardium with myocarditis caused by adriamycin.