扩张型心肌病大鼠心肌纤维化进程中TGF-β/smads信号通路激活的时相性变化及抗纤益心方干预研究

Ventricular remodeling caused by myocardial fibrosis is an important pathological basis of dilated cardiomyopathy (DCM). Documental Study indicated that TGF-β/Smads signal pathway playing an important role in the development of myocardial fibrosis with cardiovascular diseases. However, the time-related activation of TGF-β/Smads signal pathway during the development of DCM is not clear. Kangxian yixin formula which has the effect of supplementing Qi and promoting blood is an empirical formula used for the treatment of DCM in our hospital. Our previous research showed that this formula can inhibit ventricular remodeling in rat model with DCM, but the mechanism is not clear. With the purpose of enriching the DCM research system, this project study on the time-related feature of TGF-β/Smads signal pathway in rats model with DCM by observing the development of myocardial fibrosis. And then, we apply the Kangxian yixin formula to rat model with DCM, detect the cardiac function by echocardiography, and evaluate the myocardial fibrosis through related activity factor. On this basis, we make clear the regulation effect of Kangxian yixin formula on TGF-β/Smads signal pathway and providing evidence of clinical application.

心肌纤维化而致的心室重构是扩张型心肌病(DCM)的重要病理基础，文献研究表明TGF-β/Smads信号通路在心血管疾病心肌纤维化的发展过程中起着重要的作用,但在DCM发生发展的过程中，该通路的表达激活情况呈现何种时相性变化尚不清楚。抗纤益心方为我院心病科临床治疗DCM的经验方，具有益气活血的功效,前期研究表明其能够抑制DCM动物模型的心室重构，但其作用机制和途径尚待进一步明确。本课题通过观察TGF-β/Smads信号通路在DCM大鼠模型心肌纤维化进展中的时相性变化情况，来揭示DCM病理变化机制，开拓DCM研究思路，丰富DCM基础研究体系。然后通过药物干预模型并检测超声心动图、相关活性因子及心肌纤维化相关指标，来明确抗纤益心方对TGF-β/Smads信号通路的干预效果，为临床应用提供依据。