Yu, Min; Wu, Xuecheng; Wang, Jingjing; He, Mengyu; Han, Honghao; Hu, Song; Xu, Jian; Yang, Mingxia; Tan, Qi; Wang, Yanli; Wang, Hong; Xie, Weiping; Kong, Hui published the artcile< Paeoniflorin attenuates monocrotaline-induced pulmonary arterial hypertension in rats by suppressing TAK1-MAPK/NF-榄廈 pathways>, Application In Synthesis of 112-63-0, the main research area is endothelial-to-mesenchymal transition; monocrotaline; paeoniflorin; pulmonary arterial hypertension; pulmonary vascular remodeling; smooth muscle cells.
Pulmonary arterial hypertension (PAH) characterized by pulmonary vascular remodeling is a lethal disease. Paeoniflorin (PF) is a monoterpene glycoside with numerous beneficial functions, such as vasodilation, anti-inflammation and immunomodulation. This study aims to investigate the effects of PF on monocrotaline (MCT)-induced PAH rats. Our data showed that both prophylactic or therapeutic administration of PF alleviated MCT-induced increasing of right ventricular systolic pressure (RVSP), prevented right ventricle hypertrophy and pulmonary arterial remodeling, as well as inhibited inflammatory cell infiltration around pulmonary arteries. Meanwhile, PF blocked MCT-induced endothelial-mesenchymal transition (EndMT) as indicated by the restored expression of endothelial markers in lung. Moreover, PF inhibited MCT-induced down-regulation of bone morphogenetic protein receptor 2 (BMPR2) and suppressed MCT-induced phosphorylation of transforming growth factor-灏?(TGF灏? activated kinase 1 (TAK1) in vivo. In vitro studies indicated that PF prevented human pulmonary arterial smooth muscle cells (PASMCs) from platelet-derived growth factor-BB (PDGF-BB)-stimulated proliferation and migration. PF also partially reversed TGF灏?, interleukin-1灏?(IL-1灏? and tumor necrosis factor (TNF-浼? co-stimulated endothelial-to-mesenchymal transition (EndMT) in cultured human pulmonary artery endothelial cells (HPAECs). Signaling pathway anal. demonstrated that the underlying mechanism might be associated with the inhibition of TAK1-MAPK/NF-榄廈 pathways. Taken together, our results suggested that PF could be a potential drug for the treatment of PAH.
International Journal of Medical Sciences published new progress about 112-63-0. 112-63-0 belongs to class esters-buliding-blocks, and the molecular formula is C19H34O2, Application In Synthesis of 112-63-0.
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