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目的 探讨川芎嗪干预充血性心力衰竭时心房纤维化与心房颤动发生维持的分子机制。方法 选择健康成年杂种犬2 1只,随机分为正常对照组、心室快速起搏致心力衰竭组和川芎嗪干预组,观察川芎嗪干预充血性心衰实验犬心房组织I、IV型胶原(ColI、ColIV )和转化生长因子β1(TGF -β1)的mRNA表达变化。结果 川芎嗪组相对于心力衰竭组,左室射血分数明显提高,持续性心房颤动诱发率明显降低,心房颤动持续时间缩短,ColI及TGF -β1的mRNA表达下调,而ColIV在各组中无明显变化。结论 川芎嗪下调心房组织ColI和TGF -β1的mRNA表达改变,可能是其拮抗心力衰竭时心房纤维化及心房颤动发生与维持的分子机制之一。
Objective To explore the molecular mechanism of tetramethylpyrazine in the intervention of atrial fibrosis and atrial fibrillation during congestive heart failure. Methods Twenty-one healthy adult mongrel dogs were selected and randomly divided into normal control group, ventricular rapid pacemaker-induced heart failure group and tetramethylpyrazine intervention group. Tetramethylpyrazine was used to treat type I and type IV collagen in experimental dogs with congestive heart failure (ColI). , ColIV) and transforming growth factor β1 (TGF-β1) mRNA expression changes. RESULTS: Compared with the heart failure group, the tetramethylpyrazine group had significantly higher left ventricular ejection fraction, sustained reduction in the induction of atrial fibrillation, shortened duration of atrial fibrillation, and decreased mRNA expression of ColI and TGF-β1, while ColIV was absent in each group. obvious change. Conclusion The down-regulation of mRNA expression of ColI and TGF-β1 in the atrial tissue by tetramethylpyrazine may be one of the molecular mechanisms that antagonize the occurrence and maintenance of atrial fibrosis and atrial fibrillation during heart failure.