1. Qiliqiangxin Attenuates Cardiac Remodeling via Inhibition of TGF-β1/Smad3 and NF-κB Signaling Pathways in a Rat Model of Myocardial Infarction
- Author
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Qi Zheng, Anbang Han, Yizhou Zhao, Xiangning Cui, Mingjing Zhao, Yingdong Lu, and Jian Zhang
- Subjects
Male ,0301 basic medicine ,TGF-β1/Smad3 ,Physiology ,Rat model ,Myocardial Infarction ,Traditional Chinese medicine ,030204 cardiovascular system & hematology ,Collagen Type I ,NF-κB ,lcsh:Physiology ,Rats, Sprague-Dawley ,Transforming Growth Factor beta1 ,lcsh:Biochemistry ,03 medical and health sciences ,chemistry.chemical_compound ,0302 clinical medicine ,NF-KappaB Inhibitor alpha ,medicine ,Animals ,lcsh:QD415-436 ,Smad3 Protein ,Myocardial infarction ,Myocardial infarction rat ,Cardiac remodeling ,Ventricular Remodeling ,Qiliqiangxin ,lcsh:QP1-981 ,Interleukin-6 ,business.industry ,Myocardium ,Tgf β1 smad3 ,NF-kappa B ,Heart ,medicine.disease ,Actins ,Rats ,Nf κb signaling ,Disease Models, Animal ,030104 developmental biology ,chemistry ,Echocardiography ,Heart failure ,Acute Disease ,Cancer research ,business ,Drugs, Chinese Herbal ,Signal Transduction - Abstract
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-β1 (TGF-β1), phosphorylated Smad3 (p-Smad3), phosphorylated Smad7 (p-Smad7), collagen I (Col- I), alpha smooth muscle actin (a-SMA), tumor necrosis factor-α (TNF-α), interleukin 6 (IL-6), nuclear factor κB (NF-κB), and phosphorylated inhibitor of kappa B alpha (p-IκBα) were measured by western blot analysis. Results: QL treatment ameliorated adverse cardiac remodeling 8 weeks after AMI, including better preservation of cardiac function, decreased inflammation, and reduced fibrosis. In addition, QL treatment reduced Col-I, a-SMA, TGF-β1, 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-α and IL-6, as well as NF-κB and p-IκBα expression. Conclusions: QL therapy exerted protective effects against cardiac remodeling potentially by inhibiting TGF-β1/Smad3 and NF-κB signaling pathways, thereby preserving cardiac function, as well as reducing myocardial inflammation and fibrosis.
- Published
- 2018