ArticleJournal of ginseng research2016
Total ginsenosides suppress monocrotaline-induced pulmonary hypertension in rats: involvement of nitric oxide and mitogen-activated protein kinase pathways.
Article in Journal of ginseng research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Pulmonary hypertension: etiology and anti-inflammatory treatment pathways of natural products.Frontiers in pharmacology · 2025Review
- Ginseng saponin metabolite 20(S)-protopanaxadiol relieves pulmonary fibrosis by multiple-targets signaling pathways.Journal of ginseng research · 2023Article
- Traditional Herbal Medicine Discovery for the Treatment and Prevention of Pulmonary Arterial Hypertension.Frontiers in pharmacology · 2021Review
- Ginseng Compatibility Environment Attenuates Toxicity and Keeps Efficacy in Cor Pulmonale Treated by Fuzi Beimu Incompatibility Through the Coordinated Crosstalk of PKA and Epac Signaling Pathways.Frontiers in pharmacology · 2018Article
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Authors and funding
8 authors.
Funding
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Abstract
backgroundGinsenosides have been shown to exert beneficial pharmacological effects on the central nervous, cardiovascular, and endocrine systems. We sought to determine whether total ginsenosides (TG) inhibit monocrotaline (MCT)-induced pulmonary hypertension and to elucidate the underlying mechanism.
methodsMCT-intoxicated rats were treated with gradient doses of TG, with or without N (G)-nitro-l-arginine methyl ester. The levels of molecules involving the regulation of nitric oxide and mitogen-activated protein kinase pathways were determined.
resultsTG ameliorated MCT-induced pulmonary hypertension in a dose-dependent manner, as assessed by the right ventricular systolic pressure, the right ventricular hypertrophy index, and pulmonary arterial remodeling. Furthermore, TG increased the levels of pulmonary nitric oxide, endothelial nitric oxide synthase, and cyclic guanosine monophosphate. Lastly, TG increased mitogen-activated protein kinase phosphatase-1 expression and promoted the dephosphorylation of extracellular signal-regulated protein kinases 1/2, p38 mitogen-activated protein kinase, and c-Jun NH2-terminal kinase 1/2.
conclusionTG attenuates MCT-induced pulmonary hypertension, which may involve in part the regulation of nitric oxide and mitogen-activated protein kinase pathways.
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