Eupatilin alleviates right ventricular fibrosis in rats with pulmonary hypertension induced by monocrotaline.

Abstract

Pulmonary arterial hypertension (PAH) is referred to as a tumor of the cardiovascular system and is a major cause of death. It is urgent to develop safe and effective drugs to combat PAH. Eupatilin, a flavonoid extracted from Artemisia, has multiple pharmacological activities. However, the role of Eupatilin in PAH-induced right heart failure is not clear. This study was aimed to investigate the effects of Eupatilin on the PAH via monocrotaline (MCT)-induced rat models and platelet-derived growth factor-BB (PDGF-BB)-induced pulmonary artery smooth muscle cell (PASMC) model. We found Eupatilin inhibits PDGF-BB-induced proliferation of PASMCs in vitro. In addition, Eupatilin affects pulmonary blood flow and right ventricular function induced by MCT in rats. We further revealed Eupatilin alleviates pulmonary artery remodeling induced by MCT. Also, it alleviates myocardial fibrosis induced by MCT. Mechanically, Eupatilin inhibits the JNK/p38 MAPK pathway. Collectively, Eupatilin alleviates MCT-induced pulmonary vascular remodeling as well as right ventricular hypertrophy via JNK/p38 MAPK pathway and could serve as a promising drug to combat PAH.