TY - JOUR
T1 - Inhibitory effect of resveratrol on angiotensin II-induced cardiomyocyte hypertrophy
AU - Cheng, Tzu Hurng
AU - Liu, Ju Chi
AU - Lin, Heng
AU - Shih, Neng Lang
AU - Chen, Yen Ling
AU - Huang, Meng Ting
AU - Chan, Paul
AU - Cheng, Ching Feng
AU - Chen, Jin Jer
PY - 2004/2
Y1 - 2004/2
N2 - Resveratrol is proposed to account in part for the protective effect of red wine on the cardiovascular system. Angiotensin II (Ang II) is a potent hypertrophic stimulus in cardiomyocytes. In this study, we determined the effect of resveratrol on Ang II-induced cardiomyocyte hypertrophy. Cultured neonatal rat cardiomyocytes were stimulated with Ang II, and [ 3H]leucine incorporation and β-myosin heavy chain (β-MyHC) promoter activity were examined. Intracellular reactive oxygen species (ROS) were measured by a redox-sensitive fluorescent dye, 2′ 7′-dichlorofluorescin diacetate, and the extracellular signal-regulated kinase (ERK) phosphorylation was examined by Western blotting. Resveratrol inhibited Ang II-increased intracellular ROS levels. Furthermore, resveratrol, as well as the antioxidant N-acetyl-cysteine, decreased Ang II- or H 2O 2-increased protein synthesis, β-MyHC promoter activity, and ERK phosphorylation. In summary, we demonstrate for the first time that resveratrol inhibits Ang II-induced cardiomyocyte hypertrophy via attenuation of ROS generation.
AB - Resveratrol is proposed to account in part for the protective effect of red wine on the cardiovascular system. Angiotensin II (Ang II) is a potent hypertrophic stimulus in cardiomyocytes. In this study, we determined the effect of resveratrol on Ang II-induced cardiomyocyte hypertrophy. Cultured neonatal rat cardiomyocytes were stimulated with Ang II, and [ 3H]leucine incorporation and β-myosin heavy chain (β-MyHC) promoter activity were examined. Intracellular reactive oxygen species (ROS) were measured by a redox-sensitive fluorescent dye, 2′ 7′-dichlorofluorescin diacetate, and the extracellular signal-regulated kinase (ERK) phosphorylation was examined by Western blotting. Resveratrol inhibited Ang II-increased intracellular ROS levels. Furthermore, resveratrol, as well as the antioxidant N-acetyl-cysteine, decreased Ang II- or H 2O 2-increased protein synthesis, β-MyHC promoter activity, and ERK phosphorylation. In summary, we demonstrate for the first time that resveratrol inhibits Ang II-induced cardiomyocyte hypertrophy via attenuation of ROS generation.
KW - Angiotensin II
KW - Cardiomyocyte hypertrophy
KW - Extracellular signal-regulated kinase
KW - Reactive oxygen species
KW - Resveratrol
KW - β-Myosin heavy chain
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U2 - 10.1007/s00210-003-0849-6
DO - 10.1007/s00210-003-0849-6
M3 - Article
C2 - 14663554
AN - SCOPUS:1442276364
SN - 0028-1298
VL - 369
SP - 239
EP - 244
JO - Naunyn-Schmiedeberg's Archives of Pharmacology
JF - Naunyn-Schmiedeberg's Archives of Pharmacology
IS - 2
ER -