کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5823840 | 1118367 | 2012 | 14 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Potent vasodilation effect of amurensin G is mediated through the phosphorylation of endothelial nitric oxide synthase
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کلمات کلیدی
LKB1CAMK IIDAF-2NG-nitro-l-arginine methyl esterPI3-kinase/AktPP25-aminoimidazole-4-carboxamide-1-β-d-ribofuranosideeNOSNOSERKTHCMPPAMPKPI3KACCAICARPBSJnkl-NAME - L-NAMEMAPK - MAPKadenosine 5′-monophosphate-activated protein kinase - آدنوزین 5'-monophosphate-فعال پروتئین کینازACh - آهacetyl-CoA carboxylase - استیل کروکسی سیلازAcetylcholine - استیل کولینendothelial nitric oxide synthase - سنتاز اکسید نیتریک اندوتلیالPhosphate buffered saline - فسفات بافر شورPhosphatidylinositol 3-kinase - فسفاتیدیلینواستیل 3-کینازNitric oxide - نیتریک اکسیدnitric oxide synthase - نیتریک اکسید سنتازcalmodulin-dependent protein kinase II - وابسته به کالدولین پروتئین کیناز IImitogen-activated protein kinase - پروتئین کیناز فعال با mitogenextracellular signal-regulated kinase - کیناز تنظیم شده سیگنال خارج سلولیliver kinase B1 - کیناز کیناز B1Estrogen receptor - گیرنده استروژنglucocorticoid receptor - گیرنده گلوکوکورتیکوئید
موضوعات مرتبط
علوم پزشکی و سلامت
داروسازی، سم شناسی و علوم دارویی
داروشناسی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Endothelial nitric oxide synthase (eNOS) has important regulatory functions in vascular tone, and impaired endothelium-dependent vasodilatation is a key event in diabetes and atherosclerosis. Vitis amurensis grapes containing resveratrol oligomers are consumed as wine and fruit and have antioxidative and neuroprotective effects. In this study, our goal was identify the most potent eNOS-activating compound among six stilbenes and oligostilbenes found in V. amurensis and to clarify its molecular mechanism. Among the six tested compounds, amurensin G most potently relaxed endothelium-intact aortic rings and increased eNOS phosphorylation and nitric oxide (NO) production. Amurensin G increased both estrogen receptor (ER) phosphorylation and ER-dependent gene transcription, and ERα or ERβ inhibition suppressed amurensin G-mediated eNOS phosphorylation. Amurensin G enhanced the activities of phosphatidylinositol 3-kinase (PI3K) and Src and their chemical inhibitors suppressed amurensin G-stimulated eNOS phosphorylation. Moreover, amurensin G activated AMP-activated protein kinase (AMPK), and amurensin G-stimulated eNOS phosphorylation and PI3K activation were reversed by AMPK inhibition. ER inhibition reversed AMPK-dependent PI3K activation in response to amurensin G. Amurensin G-mediated endothelium-dependent relaxation was blocked by inhibition of AMPK, ER, Src, or PI3K. These results suggest that amurensin G enhances NO production via eNOS phosphorylation in endothelial cells, and ER-dependent AMPK/PI3K pathways are required. Amurensin G would be applicable to prevent atherosclerosis.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochemical Pharmacology - Volume 84, Issue 11, 1 December 2012, Pages 1437-1450
Journal: Biochemical Pharmacology - Volume 84, Issue 11, 1 December 2012, Pages 1437-1450
نویسندگان
Tran Thi Hien, Won Keun Oh, Bui Thu Quyen, Trong Tuan Dao, Jung-Hoon Yoon, Sei Young Yun, Keon Wook Kang,