Palmatine Alleviates Acute Myocardial Infarction Through Activating pAMPK/Nrf2 Signaling Pathway in Mouse Model

Abstract Acute myocardial infarction is one of the major leading causes for heart failure, which can lead to irreversible loss cardiomyocytes and impaired cardiac function. Hence, efficient therapeutic agents are still urgent. Our study aimed explore role a natural isoquinoline alkaloid, palmatine, in an acute mouse model. In this study, intragastric administrated palmatine significantly enhanced left ventricle ejection fraction end-systolic infarcted mice heart. Meanwhile, administration partially recovered structure attenuated fibrosis infiltration inflammatory cells. addition, usage further increased transforming growth factor (TGF)-beta1 level, reduced elevated tumor necrosis (TNF)-alpha interleukin (IL)-1beta level myocardium infarction–induced mice, as well superoxide dismutase production inhibited malondialdehyde secretion mice. led significant upregulation Bcl-2-associated X downregulation B-cell lymphoma-2 myocardium, statistically enabled recover expression changes these two apoptosis-related proteins. Moreover, obviously levels phosphorylated AMP-activated protein kinase nuclear erythroid 2–related 2 word, our indicated that could protect from apoptosis, inflammation, oxidative stress. results suggested might be novel agent infarction. Graphical