Qiliqiangxin Attenuates Cardiac Remodeling via Inhibition of TGF-β1/Smad3 and NF-κB Signaling Pathways in a Rat Model of Myocardial Infarction

Background/Aims: Qiliqiangxin (QL), a traditional Chinese medicine, has been demonstrated to be effective and safe for the treatment of chronic heart failure. Left ventricular (LV) remodeling causes depressed cardiac performance and is an independent determinant of morbidity and mortality after myocardial infarction (MI). Our previous studies have shown that QL exhibits cardiac protective effects against heart failure after MI. The objective of this study was to explore the effects of QL on myocardial fibrosis in rats with MI and to investigate the underlying mechanism of these effects. Methods: A rat model of acute myocardial infarction was induced by ligating the left anterior descending coronary artery. The rats were treated with QL (1.0 g/kg/day) for 4 weeks after surgery. Echocardiography and histology examination were performed to evaluate heart function and fibrosis, respectively. Protein levels of transforming growth factor-beta 1 (TGF-beta 1), phosphorylated Smad3 (p-Smad3), phosphorylated Smad7 (p-Smad7), collagen I (Col-I), alpha smooth muscle actin (a-SMA), tumor necrosis factor-alpha (TNF-alpha), interleukin 6 (IL-6), nuclear factor kappa B (NF-kappa B), and phosphorylated inhibitor of kappa B alpha (p-I kappa B alpha) were measured by western blot analysis. Results: QL treatment ameliorated adverse cardiac remodeling 8 weeks after AML including better preservation of cardiac function, decreased inflammation, and reduced fibrosis. In addition, QL treatment reduced Col-I, a-SMA, TGF-beta 1, and p-Smad3 expression levels but increased p-Smad7 levels in postmyocardial infarct rat hearts. QL administration also reduced the elevated levels of cardiac inflammation mediators, such as TNF-alpha and IL-6, as well as NE-KB and p-I kappa B alpha expression. Conclusions: QL therapy exerted protective effects against cardiac remodeling potentially by inhibiting TGF-beta 1/Smad3 and NF-kappa B signaling pathways, thereby preserving cardiac function, as well as reducing myocardial inflammation and fibrosis. (C) 2018 The Author(s) Published by Karger AG, Basel