Gallic acid attenuates oleic acid-induced proliferation of vascular smooth muscle cell through regulation of AMPK-eNOS-FAS signaling

doi:10.2174/09298673113209990175

中山醫學大學機構典藏 CSMUIR > 醫學院 > 醫學系 > 期刊論文 > Item 310902500/20407

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题名:	Gallic acid attenuates oleic acid-induced proliferation of vascular smooth muscle cell through regulation of AMPK-eNOS-FAS signaling
作者:	Ou, T.-T. Lin, M.-C. Wu, C.-H. Lin, W.-L. Wang, C.-J.
贡献者:	醫學系
关键词:	AMP-activated protein kinase (AMPK);ENOS;Gallic acid;Oleic acid;Proliferation;Vascular smooth muscle cells
日期:	2013-10
上传时间:	2019-10-24T04:23:19Z (UTC)
出版者:	Current Medicinal Chemistry
ISSN:	0929-8673
摘要:	Vascular smooth muscle cell (VSMC) proliferation plays a central role in the pathogenesis of obesity-related atherosclerosis. The molecular mechanism of GA on oleic acid (OA)-induced proliferation of vascular smooth muscle cell is evaluated. Cells were treated with OA (150 μM), or co-treated with OA and GA (10-30 μM) for 48 h, MTT assay was performed for proliferation. Using flow cytometry analysis, the GA-treated cells caused an increase in G2/M phase. A decrease in cyclin B1 and cyclin-dependent kinase 1 (cdc2) and increase in kip/p27 and cip1/p21 were found by western blotting. Additional mechanistic studies showed that GA induced the activation of AMP-activated protein kinase (AMPK) and eNOS and the inhibition of fatty acid synthase (FAS) after stimulation with OA. Furthermore, the addition of compound C, a specific inhibitor of AMPK, reduced the activation of GA-mediated eNOS and NO production and increased the proliferation of cells. Inhibition of NOS by L-NAME had no further effect on VSMC proliferation. The present results indicate that GA was an effected and anti-atherogenic agent in VSMC. It attenuates cell cycle progression via AMPKmediated eNOS activation, which results in the production of NO and prevents atherosclerosis. © 2013 Bentham Science Publishers.
URI:	https://ir.csmu.edu.tw:8080/ir/handle/310902500/20407
關聯:	Current Medicinal Chemistry, Volume 20, Issue 31, 3944-3953
显示于类别:	[醫學系] 期刊論文

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