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目的 :探讨氯沙坦、卡托普利在逆转心肌重塑中的作用及机制。方法 :Wistar大鼠 2 4只 ,随机分为 4组 ,建立心肌梗死后心肌重塑模型 ,分别为假手术组、单纯心肌梗死组、氯沙坦组和卡托普利组 ,假手术组不结扎冠状动脉。采用RT PCR方法检测c fosmRNA表达的变化 ;用免疫组织化学染色方法检测I型、III型胶原和纤维连接蛋白 (FN)表达的变化。结果 :单纯梗死组在心肌重塑时心肌c fosmRNA表达增强 ,I型、III型胶原 ,FN的表达增加 ,与假手术组比较差异有显著性意义 (P <0 .0 5或 <0 .0 1)。氯沙坦组和卡托普利组的心肌c fosmR NA表达被抑制 ,I型、III型胶原 ,FN的表达显著减弱 ,与单纯梗死组比较差异有显著性意义 (P <0 .0 5或 <0 .0 1)。结论 :氯沙坦、卡托普利均可下调原癌基因c fosmRNA的表达 ,抑制心肌间质的I型、Ⅲ型胶原和FN合成 ,具有逆转心肌重塑的作用 ,但血管紧张素Ⅱ的Ⅰ型受体阻滞剂的作用与血管紧张素转换酶抑制剂的作用相似 ,提示在临床上这两种药物可相互替换选用。
Objective: To investigate the role and mechanism of losartan and captopril in reversing myocardial remodeling. Methods: Twenty-four Wistar rats were randomly divided into 4 groups. The model of myocardial remodeling after myocardial infarction was established. They were sham-operation group, simple myocardial infarction group, losartan group and captopril group, sham operation group Coronary artery ligation. The changes of c fos mRNA expression were detected by RT PCR. The expressions of type I, type III collagen and fibronectin (FN) were detected by immunohistochemical staining. Results: The expression of c fos mRNA increased, the expression of type I, type III collagen and FN increased in myocardial infarction group compared with sham-operated group (P <0.05 or <0. 0) 1). The expression of c fosmR NA was inhibited in losartan group and captopril group, and the expression of type I, type III collagen and FN was significantly decreased, which was significantly different from those in simple infarction group (P <0.05 or <0 .0 1). CONCLUSION: Both Losartan and Captopril can down-regulate the expression of proto-oncogene c fosmRNA and inhibit the synthesis of type I, type III collagen and FN in myocardial interstitium, which can reverse myocardial remodeling. However, angiotensin II The role of type I receptor blockers and angiotensin-converting enzyme inhibitors similar role, suggesting that the two drugs in the clinical alternative to each other.