Publication: Moringa oleifera leaf extract enhances endothelial nitric oxide production leading to relaxation of resistance artery and lowering of arterial blood pressure
Issued Date
2020-10-01
Resource Type
ISSN
19506007
07533322
07533322
Other identifier(s)
2-s2.0-85089134770
Rights
Mahidol University
Rights Holder(s)
SCOPUS
Bibliographic Citation
Biomedicine and Pharmacotherapy. Vol.130, (2020)
Suggested Citation
Direk Aekthammarat, Panot Tangsucharit, Patchareewan Pannangpetch, Thanaporn Sriwantana, Nathawut Sibmooh Moringa oleifera leaf extract enhances endothelial nitric oxide production leading to relaxation of resistance artery and lowering of arterial blood pressure. Biomedicine and Pharmacotherapy. Vol.130, (2020). doi:10.1016/j.biopha.2020.110605 Retrieved from: https://repository.li.mahidol.ac.th/handle/20.500.14594/58356
Research Projects
Organizational Units
Authors
Journal Issue
Thesis
Title
Moringa oleifera leaf extract enhances endothelial nitric oxide production leading to relaxation of resistance artery and lowering of arterial blood pressure
Other Contributor(s)
Abstract
© 2020 The Authors A mass of evidence has identified a promoting of nitric oxide (NO) production in endothelial cells using natural products as a potential strategy to prevent and treat hypertension. This study investigated whether the aqueous extract of Moringa oleifera leaves (MOE) could lower mean arterial pressure (MAP) and relax mesenteric arterial beds in rats via stimulating endothelium-derived NO production. Intravenous administration of MOE (1–30 mg/kg) caused a dose-dependent reduction in MAP in anesthetized rats. In rats pretreated with the NO-synthase inhibitor, Nω-nitro-L-arginine methyl ester (L-NAME, 30 mg/kg, i.v.), the effect of MOE on MAP was significantly reduced. MOE (0.001–3 mg) induced relaxation in methoxamine (10 μM) pre-contracted mesenteric arterial beds, which was abolished by endothelium denudation. This endothelium-dependent vasorelaxation was reduced by L-NAME (100 μM) or the NO-sensitive guanylyl cyclase inhibitor, 1H- [1,2,4]-oxadiazolo-[4,3-a]-quinoxalin-1-one (10 μM). In primary human pulmonary artery endothelial cells, MOE (3–30 μg/mL) induced NO production, which was inhibited by L-NAME (100 μM) pretreatment. These findings show that MOE stimulates the endothelium-derived NO release for driving its vasorelaxation to lower arterial blood pressure. These suggest the development of MOE as a natural antihypertensive supplement.