有哪些信誉好的足球投注网站activation of the amp-activated protein kinase by eicosapentaenoic acid (epa, 205 n-3) improves endothelial function in vivo活化蛋白激酶的激活二十碳五烯酸(epa,205 n - 3)可以提高体内内皮功能.pdfVIP
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activation of the amp-activated protein kinase by eicosapentaenoic acid (epa, 205 n-3) improves endothelial function in vivo活化蛋白激酶的激活二十碳五烯酸(epa,205 n - 3)可以提高体内内皮功能
Activation of the AMP-Activated Protein Kinase by
Eicosapentaenoic Acid (EPA, 20:5 n-3) Improves
Endothelial Function In Vivo
1 1 1 1 1 2
Yong Wu , Cheng Zhang , Yunzhou Dong , Shuangxi Wang , Ping Song , Benoit Viollet , Ming-
Hui Zou1*
1 Division of Endocrinology and Diabetes, Department of Medicine, University of Oklahoma Health Science Center, Oklahoma City, Oklahoma, United States of America,
´ ´ ´ ´ ´ ´ ´ ´
2 Departement de Genetique, Developpement et Pathologie Moleculaire, Institut Cochin, Universite Rene Descartes Paris 5, Institut National de la Sante et de la Recherche
`
Medicale U567, Centre National de la Recherche Scientifique UMR8104, Paris, France
Abstract
The aim of the present study was to test the hypothesis that the cardiovascular-protective effects of eicosapentaenoic acid
(EPA) may be due, in part, to its ability to stimulate the AMP-activated protein kinase (AMPK)-induced endothelial nitric
oxide synthase (eNOS) activation. The role of AMPK in EPA-induced eNOS phosphorylation was investigated in bovine aortic
endothelial cells (BAEC), in mice deficient of either AMPKa 1 or AMPKa2, in eNOS knockout (KO) mice, or in Apo-E/AMPKa1
dual KO mice. EPA-treatment of BAEC increased both AMPK-Thr172 phosphorylation and AMPK activity, which was
accompanied by increased eNOS phosphorylation, NO release, and upregulation of mitochondrial uncoupling protein-2
(UCP-2). Pharmacologic or genetic inhibition of AMPK abolished EPA-enhanced NO release and eNOS phosphorylation in
HUVEC. This effect of EPA was absent in the aortas
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