title: Ruscogenin attenuates monocrotaline-induced pulmonary hypertension in rats.
abstract: Inflammation, endothelial dysfunction, and thrombosis contribute to the pathogenesis and development of human pulmonary arterial hypertension (PAH). The aim of this study was to investigate the effects of ruscogenin, a natural anti-inflammatory and anti-thrombotic agent, on the development of monocrotaline (MCT)-induced PAH in rats. Our results revealed that ruscogenin had favorable effects on hemodynamics and pulmonary vascular remodeling, preventing the development of PAH 3 weeks after MCT. In addition, ruscogenin resulted in markedly reduced expression of inflammatory cytokine and leukocyte infiltration via the inhibition of nuclear factor (NF)-κB activity in rat lungs. Ruscogenin also attenuated MCT-induced endothelial cell apoptosis in the remodeled pulmonary arterioles and rescued destruction of endothelial cell membrane proteins such as eNOS, caveolin-1, and CD31. Our findings suggest that ruscogenin might have therapeutic benefits for PAH patients.
authors.affiliation: Department of Geriatric Intensive Care Unit, The First Affiliated Hospital of Nanjing Medical University, Nanjing, 210029, PR China.
authors.forename: Li-Qing
authors.initials: LQ
authors.lastname: Bi
authors.forename: Rong
authors.initials: R
authors.lastname: Zhu
authors.forename: Hui
authors.initials: H
authors.lastname: Kong
authors.forename: Su-Ling
authors.initials: SL
authors.lastname: Wu
authors.forename: Nan
authors.initials: N
authors.lastname: Li
authors.forename: Xiang-Rong
authors.initials: XR
authors.lastname: Zuo
authors.forename: Su-Ming
authors.initials: SM
authors.lastname: Zhou
authors.forename: Jun-Ping
authors.initials: JP
authors.lastname: Kou
authors.forename: Bo-Yang
authors.initials: BY
authors.lastname: Yu
authors.forename: Hong
authors.initials: H
authors.lastname: Wang
authors.forename: Wei-Ping
authors.initials: WP
authors.lastname: Xie
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology / Q000627:therapeutic use*; D000959:Antihypertensive Agents / Q000494:pharmacology / Q000627:therapeutic use*; D062186:Arterial Pressure / Q000187:drug effects; D051242:Caveolin 1 / Q000378:metabolism; D004730:Endothelium, Vascular / Q000187:drug effects / Q000473:pathology; D065627:Familial Primary Pulmonary Hypertension; D006976:Hypertension, Pulmonary / Q000139:chemically induced / Q000188:drug therapy* / Q000473:pathology / Q000503:physiopathology; D053583:Interleukin-1beta / Q000378:metabolism; D008297:Male; D016686:Monocrotaline; D016328:NF-kappa B / Q000378:metabolism; D052250:Nitric Oxide Synthase Type III / Q000378:metabolism; D019408:Platelet Endothelial Cell Adhesion Molecule-1 / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D013150:Spirostans / Q000494:pharmacology / Q000627:therapeutic use*; D013925:Thromboplastin / Q000378:metabolism
chemical_list: D000893:Anti-Inflammatory Agents; D000959:Antihypertensive Agents; D051242:Caveolin 1; D053583:Interleukin-1beta; D016328:NF-kappa B; D019408:Platelet Endothelial Cell Adhesion Molecule-1; D013150:Spirostans; D016686:Monocrotaline; D013925:Thromboplastin; C012541:ruscogenin; D052250:Nitric Oxide Synthase Type III; C496316:Nos3 protein, rat