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http://dx.doi.org/10.4196/kjpp.2022.26.2.87

Peiminine inhibits myocardial injury and fibrosis after myocardial infarction in rats by regulating mitogen-activated protein kinase pathway  

Chen, Peng (Department of Vasculocardiology, Xiangyang Central Hospital, Affiliated Hospital of Hubei University of Arts and Science)
Zhou, Dengming (Department of Vasculocardiology, Xiangyang Central Hospital, Affiliated Hospital of Hubei University of Arts and Science)
Liu, Yongsheng (Department of Vasculocardiology, Xiangyang Central Hospital, Affiliated Hospital of Hubei University of Arts and Science)
Wang, Ping (Department of Vasculocardiology, Xiangyang Central Hospital, Affiliated Hospital of Hubei University of Arts and Science)
Wang, Weina (Department of Vasculocardiology, Xiangyang Central Hospital, Affiliated Hospital of Hubei University of Arts and Science)
Publication Information
The Korean Journal of Physiology and Pharmacology / v.26, no.2, 2022 , pp. 87-94 More about this Journal
Abstract
Myocardial infarction promotes cardiac remodeling and myocardial fibrosis, thus leading to cardiac dysfunction or heart failure. Peiminine has been regarded as a traditional anti-fibrotic Chinese medicine in pulmonary fibrosis. However, the role of peiminine in myocardial infarction-induced myocardial injury and fibrosis remained elusive. Firstly, rat model of myocardial infarction was established using ligation of the left coronary artery, which were then intraperitoneally injected with 2 or 5 mg/kg peiminine once a day for 4 weeks. Echocardiography and haemodynamic evaluation results showed that peiminine treatment reduced left ventricular end-diastolic pressure, and enhanced maximum rate of increase/decrease of left ventricle pressure (± dP/dt max) and left ventricular systolic pressure, which ameliorate the cardiac function. Secondly, myocardial infarction-induced myocardial injury and infarct size were also attenuated by peiminine. Moreover, peiminine inhibited myocardial infarction-induced increase of interleukin (IL)-1β, IL-6 and tumor necrosis factor-α production, as well as the myocardial cell apoptosis, in the rats. Thirdly, peiminine also decreased the myocardial fibrosis related protein expression including collagen I and collagen III. Lastly, peiminine reduced the expression of p38 and phosphorylation of extracellular signal-regulated kinase 1/2 in rat model of myocardial infarction. In conclusion, peiminine has a cardioprotective effect against myocardial infarction-induced myocardial injury and fibrosis, which can be attributed to the inactivation of mitogen-activated protein kinase pathway.
Keywords
Fibrosis; Mitogen-activated protein kinase; Myocardial infarction; Myocardial injury; Peiminine;
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