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Publication Details
AFRICAN RESEARCH NEXUS
SHINING A SPOTLIGHT ON AFRICAN RESEARCH
biochemistry, genetics and molecular biology
Notoginsenoside Ft1 activates both glucocorticoid and estrogen receptors to induce endothelium-dependent, nitric oxide-mediated relaxations in rat mesenteric arteries
Biochemical Pharmacology, Volume 88, No. 1, Year 2014
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Description
Panax notoginseng (Burk.) F.H. Chen has been used traditionally for the treatment of cardiovascular diseases. Notoginsenoside Ft1 (Ft1) is a bioactive saponin from the leaves of P. notoginseng. Experiments were designed to determine whether or not Ft1 is an endothelium-dependent vasodilator. Rat mesenteric arteries were suspended in organ chambers for the measurement of isometric tension during phenylephrine-induced contractions. The cyclic guanosine monophosphate (cGMP) level was assessed using enzyme immunoassay. The phosphorylation and protein expressions of endothelial nitric oxide synthase (eNOS), glucocorticoid receptors (GR), estrogen receptors beta (ERß), protein kinase B (Akt) and extracellular signal-regulated kinase 1/2 (ERK1/2) were determined by Western blotting. The localization of GR and ERß were determined by immunofluorescence staining. Ft1 caused endothelium-dependent relaxations, which were abolished by l-NAME (inhibitor of nitric oxide synthases) and ODQ (inhibitor of soluble guanylyl cyclase). Ft1 increased the cGMP level in rat mesenteric arteries. GR and ERß were present in the endothelial layer and their antagonism by RU486 and PHTPP, respectively, inhibited Ft1-induced endothelium-dependent relaxations and phosphorylations of eNOS, Akt and ERK1/2. Inhibition of phosphoinositide-3-kinase (PI3K) by wortmannin and ERK1/2 by U0126 reduced Ft1-evoked relaxations and eNOS phosphorylation. Taken in conjunction, the present findings suggest that Ft1 stimulates endothelial GRs and ERßs with subsequent activation of the PI3K/Akt and ERK1/2 pathways in rat mesenteric arteries. This results in phosphorylation of eNOS and the release of NO, which activates soluble guanylyl cyclase in the vascular smooth muscle cells leading to relaxations. © 2014 Elsevier Inc.
Authors & Co-Authors
Shen, Kaikai
China, Shanghai
Shanghai University of Traditional Chinese Medicine
Hong Kong
The University of Hong Kong Li ka Shing Faculty of Medicine
Leung, Susan Wai Sum
Hong Kong
The University of Hong Kong Li ka Shing Faculty of Medicine
Ji, Lili
China, Shanghai
Shanghai University of Traditional Chinese Medicine
Huang, Yu
Hong Kong, Hong Kong
Chinese University of Hong Kong
Hou, Maoqi
China, Shanghai
Shanghai University of Traditional Chinese Medicine
Xu, Aimin
Hong Kong
The University of Hong Kong Li ka Shing Faculty of Medicine
Wang, Zhengtao
China, Shanghai
Shanghai University of Traditional Chinese Medicine
Vanhoutte, Paul M.
Hong Kong
The University of Hong Kong Li ka Shing Faculty of Medicine
Saudi Arabia, Riyadh
College of Pharmacy
Statistics
Citations: 29
Authors: 8
Affiliations: 4
Identifiers
Doi:
10.1016/j.bcp.2014.01.007
ISSN:
00062952
e-ISSN:
18732968
Research Areas
Noncommunicable Diseases