摘要
目的探讨曲美他嗪对急性心肌梗死(AMI)模型大鼠梗死区、非梗死区胶原蛋白分子表达的影响。方法将结扎冠状动脉左前降支AMI鼠48只随机分成模型组、倍他乐克(琥珀酸美托洛尔)组(2 mg.kg-1.d-1)、曲美他嗪组(10 mg.kg-1.d-1)。另设假手术组。同步药物干预8 w后,RT-PCR检测梗死区胶原-Ⅰ mRNA。结果与模型组比较,倍他乐克组、曲美他嗪组梗死区胶原-Ⅰ mRNA表达均明显下调(P<0.05);倍他乐克组与曲美他嗪组水平接近,差别不显著(P>0.05)。与模型组比较,倍他乐克组、曲美他嗪组非梗死区胶原-Ⅰ mRNA表达均明显下调(P<0.05);倍他乐克组与曲美他嗪组表达水平接近,差别不显著(P>0.05)。结论曲美他嗪既能减少AMI大鼠梗死区胶原分子的合成又能减少非梗死区胶原分子的合成,可有效延缓整个心肌纤维化的进程。
Objective To study the effect of trimetazidine on the production of collagen in acute myocardial infarction（AMI） rat.Methods 48 rats surviving left anterior descending coronary artery ligation were randomly divided into AMI model,metoprolol（2 mg·kg-1·d-1） and trimetazidine（10 mg·kg-1·d-1） with additional eight other rats being sham.Eight weeks later,the expressions of collagen types Ⅰ（collagen I） were measured by RT-PCR both in infarct zone（IZ） and non-infarct zone（NIZ）.Results Compared with those of sham rats,the expressions of collagen Ⅰ of model rats and the other two admission groups were evidently increased（P﹤0.05）.Compared with those of model rats,the expressions were down-regulated in metoprolol rats and trimetazidine rats.There were no significant differences between metoprolol and trimetazidine rats（P﹥0.05）.The expressions collagen Ⅰ in NIZ were as follow：compared with those of sham rats,the expressions of model rats and the other two admission groups were evidently increased（P﹤0.05）.Compared with those of model rats,the expressions were down-regulated in metoprolol and trimetazidine rats,but having no significant differences between the two admission groups（P﹥0.05）.Conclusions Trimetazidine could significantly inhibit the production of collage in both IZ and NIZ.Trimetazidine could effectively delay the course of myocardial fibrosis.
出处
《中国老年学杂志》
CAS
CSCD
北大核心
2011年第15期2870-2872,共3页
Chinese Journal of Gerontology
基金
国家自然科学基金资助项目(No.30770883)
关键词
急性心肌梗死
曲美他嗪
胶原-Ⅰ
心肌纤维化
Acute myocardial infarction（AMI）
Trimetazidine
Collagen-I
Myocardial fibrosis
