Quercetin regulates pulmonary vascular remodeling in pulmonary hypertension through TGF-β1-Smad2/3 pathway

Abstract

Abstract Pulmonary arterial hypertension (PAH) is a rare, poorly prognostic, fatal progressive disease characterized by progressively elevated pulmonary artery pressure. We investigated the pharmacological action and mechanism of quercetin on pulmonary hypertension, since the existing therapeutic drugs could not stop the disease progression. In this paper, the mechanism of quercetin's protective effect on pulmonary hypertension was investigated by in vivo and cell experiments. Our results suggest that quercetin therapy alleviates pulmonary hypertension, reduces right ventricular hypertrophy, and improves pulmonary remodeling in monocrotaline (MCT) -induced pulmonary hypertension in rats, possibly by inhibiting the TGF-β1/ Smad2/3 signaling pathway. In addition, quercetin can effectively inhibit the proliferation, migration and phenotype transformation of human pulmonary artery smooth muscle cells (HPASMCs) induced by platelet-derived growth factor BB (PDGF-BB), and its mechanism may also be related to the above signal pathways. In short, this study suggests that quercetin may serve as a potential treatment for PAH, possibly through the TGF-β1/ Smad2/3 signaling pathway.