Inhibitiory effect of trilinolein on endothelin-1-induced c-fos gene expression in cultured neonatal rat cardiomyocytes

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TMUIR > College of Medicine > Department of Medicine > Department of Surgery > Periodical Article > Item 987654321/13545

Please use this identifier to cite or link to this item: http://libir.tmu.edu.tw/handle/987654321/13545

Title:	Inhibitiory effect of trilinolein on endothelin-1-induced c-fos gene expression in cultured neonatal rat cardiomyocytes
Authors:	林家瑋 Hung-Yu Yang;Ju-Chi Liu;Yen-Ling Chen;Cheng-Hsien Chen;Heng Lin;Jia-Wei Lin;Wen-Ta Chiu;Jin-Jer Chen;Tzu-Hurng C
Contributors:	醫學系外科學科
Date:	2005
Issue Date:	2009-10-28 12:15:17 (UTC+8)
Abstract:	Trilinolein, isolated from the traditional Chinese herb Sanchi (Panax notoginseng), has been shown to have myocardial protective effects via its antioxidant ability. However, the cellular and molecular mechanisms of the protective effect of trilinolein in the heart remain to be elucidated. Oxidative mechanisms have been implicated in neonatal cardiomyocyte hypertrophy. We previously reported that ET-1 induces ROS generation via the ETA receptor and ROS modulates c-fos gene expression. We have therefore examined whether trilinolein attenuates ROS production and ET-1-induced c-fos gene expression in cardiomyocytes. Cultured neonatal rat cardiomyocytes were stimulated with ET-1 (10 nM), and c-fos gene expression was examined. Trilinolein (1 and 10 μM) inhibited ET-1-induced c-fos gene expression in cardiomyocytes. We also examined the effects of trilinolein on ET-1- increased NADPH oxidase activity and superoxide formation. Trilinolein inhibited ET-1-increased NADPH oxidase activity and superoxide formation in a concentration- dependent manner. This increase in superoxide production by ET-1 was significantly inhibited by trilinolein, diphenyleneiodonium, or N-acetylcysteine. Trilinolein also decreased ET-1- or H2O2-induced extracellular signalregulated kinase (ERK) phosphorylation, c-Jun NH2- terminal kinase (JNK) phosphorylation, and activator protein-1 activation. These data indicate that trilinolein inhibits ET-1-induced ERK phosphorylation, JNK phosphorylation, and c-fos gene expression via attenuating superoxide production in cardiomyocytes. Keywords Trilinolein . Endothelin-1 . Cardiomyocyte hypertrophy . Superoxide . Signal transduction . Gene expression
Relation:	Naunyn-Schmiedeberg’s Arch Pharmacol.(372):160-167.
Data Type:	article
Appears in Collections:	[Department of Surgery] Periodical Article

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