Qiliqiangxin attenuates isoproterenol-induced cardiac remodeling in mice.

Background: To further explore the role of PPAR. in QL treatment, ISO-induced mice model and following methods were established. Methods: Cardiac remodeling on mice model was induced by isoproterenol (ISO) infusion or saline infusion as control for two weeks then divided into 4 groups, after that divided in 5 different treatment methods to investigate the role of PPAR. in QL therapy. Echocardiography and Masson's trichrome staining were respectively used to determine cardiac function and fibrosis. Immunoblotting was applied to evaluate the expression levels of proliferator-activated receptor-gamma (PPAR gamma), Bax, Bcl, phospho-Akt (Ser473), Akt, phospho-P38 and P38, phosphor-ERK and ERK. Results: QL treatment improved left ventricular function, decreased apoptosis, and prevented myocardial fibrosis at the same time. Meanwhile, the PPAR. level was elevated with QL treatment in ISO-injected mice hearts. Inhibition of PPAR gamma activity blocked the protective effects of QL, while the activator of PPAR. did not provide additional benefit. Specifically, the results indicated a decline in PPAR. in ISO-infused mice and QL decreased the toxicity of ISO by improving the level of PPAR gamma. Conclusions: Our study demonstrated that QL treatment provided cardioprotection against ISO-induced cardiac remodeling by improving PPAR. level, which could be as the potential therapeutic target in reversing cardiac remodeling and heart failure.