Kangxian Yixin Formula improved cardiac function and reduced myocardial fibrosis in mice with dilated cardiomyopathy, significantly down-regulating MCU, CaM, NFAT4, and α-SMA expression (P<0.05).
RCT (n=50)
Randomly divided
Does Kangxian Yixin Formula improve myocardial fibrosis and cardiac function in a mouse model of dilated cardiomyopathy?
Kangxian Yixin Formula attenuates myocardial fibrosis and improves cardiac function in a mouse model of dilated cardiomyopathy, potentially by modulating the MCU pathway.
valor p: p=<0.05
目的 探讨抗纤益心方对扩张型心肌病（DCM）小鼠心肌纤维化的影响。 方法 将40只DCM小鼠随机分为模型组、抗纤益心方组、卡托普利组及抗纤益心方合卡托普利组，每组10只，另设10只正常组对照。药物干预8周后，采用超声心动图评估心功能，HE与Masson染色观察心肌病理与纤维化，透射电镜观察线粒体结构，PCR与Western blot检测线粒体钙单向转运体（MCU）、钙调蛋白（CaM）、活化T细胞核因子4（NFAT4）、I型胶原蛋白（COL-1）及α-平滑肌肌动蛋白（α-SMA）的表达。 结果 与正常组比较，模型组心功能下降（LVEDd升高，LVEF、LVFS降低），心肌排列紊乱、纤维化明显，线粒体结构损伤，与模型组比较，抗纤益心方组心功能改善，纤维化减轻，线粒体损伤缓解，MCU、CaM、NFAT4、α-SMA的mRNA或蛋白表达均显著下调（PPP 结论 抗纤益心方能够减轻DCM小鼠心肌纤维化，改善心功能，其作用机制可能与MCU通路调控水平有关。
HE et al. (Sun,) conducted a rct in Dilated cardiomyopathy (DCM) (n=50). Kangxian Yixin Formula vs. Model group, captopril group, and normal control was evaluated on Cardiac function, myocardial fibrosis, and MCU pathway protein expression (p=<0.05). Kangxian Yixin Formula improved cardiac function and reduced myocardial fibrosis in mice with dilated cardiomyopathy, significantly down-regulating MCU, CaM, NFAT4, and α-SMA expression (P<0.05).