TY - JOUR
T1 - The inhibitory effect of trilinolein on norepinephrine-induced β-myosin heavy chain promoter activity, reactive oxygen species generation, and extracellular signal-regulated kinase phosphorylation in neonatal rat cardiomyocytes
AU - Liu, Ju Chi
AU - Chan, Paul
AU - Chen, Jin Jer
AU - Lee, Horng Mo
AU - Lee, Wen Sen
AU - Shih, Neng Lang
AU - Chen, Yen Ling
AU - Hong, Hong Jye
AU - Cheng, Tzu-Hurng
PY - 2004
Y1 - 2004
N2 - The myocardial protective effects of trilinolein, isolated from the traditional Chinese herb Sanchi (Panax notoginseng),are thought to be related to its antioxidant activity. However, the intracellular mechanism underlying the protective effect of trilinolein in the heart remains unclear. In the present study, we investigated the effect of trilinolein on norepinephrine (NE)-induced protein synthesis in cardiomyocytes. Cultured neonatal rat cardiomyocytes were stimulated with NE, then protein content, [ 3H]-leucine incorporation, and β-myosin heavy chain (β-MyHC) promoter activity were examined. The effect of trilinolein on NE-induced intracellular reactive oxygen species (ROS) generation was measured with a redox-sensitive fluorescent dye (2′,7′-dichlorofluorescin diacetate) and extracellular signal-regulated kinase (ERK) phosphorylation by Western blotting. Trilinolein inhibited NE-increased protein synthesis, β-MyHC promoter activity, and intracellular ROS. Both trilinolein and the antioxidant, N-acetyl-cysteine, decreased NE- and H2O 2-induced protein synthesis, β-MyHC promoter activity, and ERK phosphorylation. These data indicate that trilinolein inhibits NE-induced protein synthesis via attenuation of ROS generation in cardiomyocytes.
AB - The myocardial protective effects of trilinolein, isolated from the traditional Chinese herb Sanchi (Panax notoginseng),are thought to be related to its antioxidant activity. However, the intracellular mechanism underlying the protective effect of trilinolein in the heart remains unclear. In the present study, we investigated the effect of trilinolein on norepinephrine (NE)-induced protein synthesis in cardiomyocytes. Cultured neonatal rat cardiomyocytes were stimulated with NE, then protein content, [ 3H]-leucine incorporation, and β-myosin heavy chain (β-MyHC) promoter activity were examined. The effect of trilinolein on NE-induced intracellular reactive oxygen species (ROS) generation was measured with a redox-sensitive fluorescent dye (2′,7′-dichlorofluorescin diacetate) and extracellular signal-regulated kinase (ERK) phosphorylation by Western blotting. Trilinolein inhibited NE-increased protein synthesis, β-MyHC promoter activity, and intracellular ROS. Both trilinolein and the antioxidant, N-acetyl-cysteine, decreased NE- and H2O 2-induced protein synthesis, β-MyHC promoter activity, and ERK phosphorylation. These data indicate that trilinolein inhibits NE-induced protein synthesis via attenuation of ROS generation in cardiomyocytes.
KW - β-Myosin heavy chain gene
KW - Extracellular signal-regulated kinase
KW - Norepinephrine
KW - Reactive oxygen species
KW - Trilinolein
UR - http://www.scopus.com/inward/record.url?scp=0942289907&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0942289907&partnerID=8YFLogxK
U2 - 10.1159/000075284
DO - 10.1159/000075284
M3 - Article
C2 - 14730205
AN - SCOPUS:0942289907
VL - 11
SP - 11
EP - 18
JO - Journal of Biomedical Science
JF - Journal of Biomedical Science
SN - 1021-7770
IS - 1
ER -