论文部分内容阅读
目的通过研究血塞通在大鼠急性心梗后心肌重塑中的干预作用及对TGF-β1/Smads通路的影响,探讨血塞通对急性心梗后心肌重塑的效应机制,为血塞通治疗急性心梗后心肌重塑提供实验依据。方法清洁级Wistar雄性大鼠50只随机分为5组,分别为正常组、模型组、假手术组、血塞通组、基质细胞衍生因子-1受体阻断剂(AMD3100)组,每组10只。血塞通组大鼠术前3天给药,1次/d。7 d后,实时荧光定量RT-PCR检测心肌组织转化生长因子(TGF)β1mRNA、Smad3mRNA、Smad7mRNA表达,分析各组非梗死区心肌胶原含量,并观察心肌组织HE染色结果。结果与假手术组相比较,模型组心肌组织TGF-β1mRNA、Smad3mRNA表达均增加(P<0.05),而Smad7mRNA表达降低(P<0.05)。与模型组相比较,血塞通组能降低心肌组织TGF-β1mRNA、Smad3mRNA表达(P<0.05),增加Smad7mRNA表达(P<0.05),降低心肌胶原含量,并能减轻心肌组织的病理损伤。血塞通组与AMD3100组相比较,TGF-β1mRNA、Smad3mRNA、Smad7mRNA表达均无明显差异(P>0.05)。结论血塞通对急性心梗后心肌重塑有一定抑制作用。
Objective To study the effect of Xuesaitong in myocardial remodeling after acute myocardial infarction in rats and its effect on TGF-β1 / Smads pathway, and to explore the mechanism of Xuesaitong in myocardial remodeling after acute myocardial infarction. To provide experimental evidence for myocardial remodeling after acute myocardial infarction. Methods Fifty clean Wistar male rats were randomly divided into 5 groups: normal group, model group, sham operation group, Xuesaitong group, and stromal cell-derived factor-1 receptor blocker (AMD3100) 10 only Xuesaitong group rats were given 3 days before operation, once a day. After 7 days, the expression of TGFβ1mRNA, Smad3mRNA and Smad7mRNA in myocardial tissue were detected by real-time fluorescent quantitative RT-PCR. The myocardial collagen content in non-infarcted area of each group was analyzed, and the myocardial tissue HE staining was observed. Results Compared with the sham operation group, the expression of TGF-β1mRNA and Smad3mRNA in the model group increased (P <0.05), while the expression of Smad7mRNA decreased (P <0.05). Compared with the model group, Xuesaitong group could decrease the expression of TGF-β1mRNA and Smad3mRNA, increase the expression of Smad7mRNA (P <0.05), decrease the content of myocardial collagen, and alleviate the myocardial injury. Compared with AMD3100 group, there was no significant difference in the expression of TGF-β1mRNA, Smad3mRNA and Smad7mRNA in Xuesaitong group (P> 0.05). Conclusion Xuesaitong can inhibit myocardial remodeling after acute myocardial infarction.