Molecular mechanism of the inhibitory effect of trilinolein on endothelin-1-induced hypertrophy of cultured neonatal rat cardiomyocytes

Shi Chung Chen, Jun Jack Cheng, Ming Hsiung Hsieh, Yen Ling Chu, Pai Feng Kao, Tzu-Hurng Cheng, Paul Chan

研究成果: 雜誌貢獻文章

14 引文 (Scopus)

摘要

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 therefore have examined whether trilinolein attenuates reactive oxygen species (ROS) production and thus ET-1-induced hypertrophy of cardiomyocytes, Cultured neonatal rat cardiomyocytes were stimulated with ET-1 (10 nM), [ 3H]leucine incorporation and the β-myosin heavy chain (β-MyHC) promoter activity were examined. Trilinolein (1 and 10 μM) inhibited the ET-1-induced increase of [3H]-leucine incorporation in a concentration-dependent manner. Trilinolein (1 and 10 μM) also inhibited ET-1-induced β-MyHC promoter activity in cardiomyocytes. We further examined the effects of trilinolein on ET-1-induced intracellular ROS generation by measuring a redox-sensitive fluorescent dye, 2′,7′- dichlorofluorescin diacetate, fluorescence intensity. Trilinolein (1 and 10 μM) inhibited ET-1-increased intracellular ROS levels in a concentration-dependent manner. This increase of ROS by ET-1 (10 μM) or H2O2 (25 μM) was significantly inhibited by trilinolein (10 μM) and N-acetylcysteine (10 mM). Moreover, ET-1-or H2O 2-induced β-MyHC promoter activity and protein synthesis were also inhibited by trilinolein (10 μM). These data indicate that trilinolein inhibits ET-1-induced β-MyHC promoter activity, and subsequent hypertrophy via its antioxidant ability in cardiomyocytes.
原文英語
頁(從 - 到)525-529
頁數5
期刊Planta Medica
71
發行號6
DOIs
出版狀態已發佈 - 六月 2005

指紋

endothelins
Endothelin-1
hypertrophy
Cardiac Myocytes
Hypertrophy
Rats
neonates
reactive oxygen species
promoter regions
leucine
protective effect
Reactive Oxygen Species
Panax notoginseng
antioxidants
acetylcysteine
myosin heavy chains
fluorescent dyes
Leucine
herbs
Antioxidants

ASJC Scopus subject areas

  • Plant Science
  • Drug Discovery
  • Organic Chemistry
  • Pharmacology

引用此文

Molecular mechanism of the inhibitory effect of trilinolein on endothelin-1-induced hypertrophy of cultured neonatal rat cardiomyocytes. / Chen, Shi Chung; Cheng, Jun Jack; Hsieh, Ming Hsiung; Chu, Yen Ling; Kao, Pai Feng; Cheng, Tzu-Hurng; Chan, Paul.

於: Planta Medica, 卷 71, 編號 6, 06.2005, p. 525-529.

研究成果: 雜誌貢獻文章

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title = "Molecular mechanism of the inhibitory effect of trilinolein on endothelin-1-induced hypertrophy of cultured neonatal rat cardiomyocytes",
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 therefore have examined whether trilinolein attenuates reactive oxygen species (ROS) production and thus ET-1-induced hypertrophy of cardiomyocytes, Cultured neonatal rat cardiomyocytes were stimulated with ET-1 (10 nM), [ 3H]leucine incorporation and the β-myosin heavy chain (β-MyHC) promoter activity were examined. Trilinolein (1 and 10 μM) inhibited the ET-1-induced increase of [3H]-leucine incorporation in a concentration-dependent manner. Trilinolein (1 and 10 μM) also inhibited ET-1-induced β-MyHC promoter activity in cardiomyocytes. We further examined the effects of trilinolein on ET-1-induced intracellular ROS generation by measuring a redox-sensitive fluorescent dye, 2′,7′- dichlorofluorescin diacetate, fluorescence intensity. Trilinolein (1 and 10 μM) inhibited ET-1-increased intracellular ROS levels in a concentration-dependent manner. This increase of ROS by ET-1 (10 μM) or H2O2 (25 μM) was significantly inhibited by trilinolein (10 μM) and N-acetylcysteine (10 mM). Moreover, ET-1-or H2O 2-induced β-MyHC promoter activity and protein synthesis were also inhibited by trilinolein (10 μM). These data indicate that trilinolein inhibits ET-1-induced β-MyHC promoter activity, and subsequent hypertrophy via its antioxidant ability in cardiomyocytes.",
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author = "Chen, {Shi Chung} and Cheng, {Jun Jack} and Hsieh, {Ming Hsiung} and Chu, {Yen Ling} and Kao, {Pai Feng} and Tzu-Hurng Cheng and Paul Chan",
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T1 - Molecular mechanism of the inhibitory effect of trilinolein on endothelin-1-induced hypertrophy of cultured neonatal rat cardiomyocytes

AU - Chen, Shi Chung

AU - Cheng, Jun Jack

AU - Hsieh, Ming Hsiung

AU - Chu, Yen Ling

AU - Kao, Pai Feng

AU - Cheng, Tzu-Hurng

AU - Chan, Paul

PY - 2005/6

Y1 - 2005/6

N2 - 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 therefore have examined whether trilinolein attenuates reactive oxygen species (ROS) production and thus ET-1-induced hypertrophy of cardiomyocytes, Cultured neonatal rat cardiomyocytes were stimulated with ET-1 (10 nM), [ 3H]leucine incorporation and the β-myosin heavy chain (β-MyHC) promoter activity were examined. Trilinolein (1 and 10 μM) inhibited the ET-1-induced increase of [3H]-leucine incorporation in a concentration-dependent manner. Trilinolein (1 and 10 μM) also inhibited ET-1-induced β-MyHC promoter activity in cardiomyocytes. We further examined the effects of trilinolein on ET-1-induced intracellular ROS generation by measuring a redox-sensitive fluorescent dye, 2′,7′- dichlorofluorescin diacetate, fluorescence intensity. Trilinolein (1 and 10 μM) inhibited ET-1-increased intracellular ROS levels in a concentration-dependent manner. This increase of ROS by ET-1 (10 μM) or H2O2 (25 μM) was significantly inhibited by trilinolein (10 μM) and N-acetylcysteine (10 mM). Moreover, ET-1-or H2O 2-induced β-MyHC promoter activity and protein synthesis were also inhibited by trilinolein (10 μM). These data indicate that trilinolein inhibits ET-1-induced β-MyHC promoter activity, and subsequent hypertrophy via its antioxidant ability in cardiomyocytes.

AB - 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 therefore have examined whether trilinolein attenuates reactive oxygen species (ROS) production and thus ET-1-induced hypertrophy of cardiomyocytes, Cultured neonatal rat cardiomyocytes were stimulated with ET-1 (10 nM), [ 3H]leucine incorporation and the β-myosin heavy chain (β-MyHC) promoter activity were examined. Trilinolein (1 and 10 μM) inhibited the ET-1-induced increase of [3H]-leucine incorporation in a concentration-dependent manner. Trilinolein (1 and 10 μM) also inhibited ET-1-induced β-MyHC promoter activity in cardiomyocytes. We further examined the effects of trilinolein on ET-1-induced intracellular ROS generation by measuring a redox-sensitive fluorescent dye, 2′,7′- dichlorofluorescin diacetate, fluorescence intensity. Trilinolein (1 and 10 μM) inhibited ET-1-increased intracellular ROS levels in a concentration-dependent manner. This increase of ROS by ET-1 (10 μM) or H2O2 (25 μM) was significantly inhibited by trilinolein (10 μM) and N-acetylcysteine (10 mM). Moreover, ET-1-or H2O 2-induced β-MyHC promoter activity and protein synthesis were also inhibited by trilinolein (10 μM). These data indicate that trilinolein inhibits ET-1-induced β-MyHC promoter activity, and subsequent hypertrophy via its antioxidant ability in cardiomyocytes.

KW - Cardiomyocyte hypertrophy

KW - Endothelin-1

KW - Reactive oxygen species

KW - Trilinolein

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DO - 10.1055/s-2005-864153

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