peoniflorin has been researched along with Pulmonary-Arterial-Hypertension* in 2 studies
2 other study(ies) available for peoniflorin and Pulmonary-Arterial-Hypertension
| Article | Year |
|---|---|
Paeoniflorin attenuates monocrotaline-induced pulmonary arterial hypertension in rats by suppressing TAK1-MAPK/NF-κB pathways.
Topics: Animals; Disease Models, Animal; Endothelial Cells; Glucosides; Hypertension, Pulmonary; MAP Kinase Kinase Kinases; Monocrotaline; Monoterpenes; NF-kappa B; Pulmonary Arterial Hypertension; Pulmonary Artery; Rats | 2022 |
Paeoniflorin Ameliorates Chronic Hypoxia/SU5416-Induced Pulmonary Arterial Hypertension by Inhibiting Endothelial-to-Mesenchymal Transition.
Endothelial cells dysfunction is one of the hallmark pathogenic features of pulmonary arterial hypertension (PAH). Paeoniflorin (PF) is a monoterpene glycoside with endothelial protection, vasodilation, antifibrotic, anti-inflammatory and antioxidative properties. However, the effects of PF on PAH remain unknown.. Here, we investigated the efficacy of PF in the SU5416/hypoxia (SuHx) rat model of PAH. Human pulmonary arterial endothelial cells (HPAECs) were exposed to 1% O. Hemodynamics analysis showed that prophylactic treatment with PF (300 mg/kg i.g. daily for 21 days) significantly inhibited chronic hypoxia/SU5416-induced elevations of right ventricular systolic pressure (RVSP) and right ventricular hypertrophy index in rats. Meanwhile, PF significantly reduced pulmonary vascular remodeling, as well as alleviated collagen deposition in lungs and right ventricles in SuHx rats. Additionally, PF inhibited SuHx-induced down-regulation of endothelial marker (vascular endothelial cadherin) and up-regulation of mesenchymal markers (fibronectin and vimentin) in lung, suggesting that PF could inhibit SuHx-induced endothelial-to-mesenchymal transition (EndMT) in lung. Further in vitro studies confirmed that PF treatment suppressed hypoxia-induced EndMT in HPAECs, which was abolished by the knockdown of bone morphogenetic protein receptor type 2 (BMPR2) in HPAECs.. Taken together, our findings suggest that PF ameliorates BMPR2 down-regulation-mediated EndMT and thereafter alleviates SuHx-induced PAH in rats. Topics: Animals; Cells, Cultured; Chronic Disease; Disease Models, Animal; Endothelial Cells; Epithelial-Mesenchymal Transition; Glucosides; Humans; Hypoxia; Indoles; Injections, Subcutaneous; Male; Monoterpenes; Oxygen; Pulmonary Arterial Hypertension; Pyrroles; Rats; Rats, Sprague-Dawley | 2020 |