From the Department of Cardiovascular Medicine (K.N., H.K., T.O.),
Department of Anatomy (K.N.), and Department of Cell Biology, Institute of
Molecular and Cellular Biology (K.F., K.M., M.M., M.N.), Okayama University
Medical School, Japan.
Correspondence to Kazufumi Nakamura, MD, Department of Cardiovascular Medicine, Okayama University Medical School, 2–5-1 Shikata, Okayama 700-8558, Japan. E-mail cardio{at}cc.okayama-u.ac.jp
Background—Tumor necrosis factor-
Methods and Results—To test the hypothesis, we tested
whether TNF-
Conclusions—These results indicate that TNF-
© 1998 American Heart Association, Inc.
Basic Science Reports
Inhibitory Effects of Antioxidants on Neonatal Rat Cardiac Myocyte Hypertrophy Induced by Tumor Necrosis Factor-
and Angiotensin II
(TNF-) and angiotensin II (Ang II) modulate heart
failure in part by provoking the hypertrophic response. Signal
transduction pathways of those factors are implicated in reactive
oxygen intermediates (ROIs). Therefore, we hypothesized that TNF-
and Ang II might cause myocyte hypertrophy via the
generation of ROIs. and Ang II could induce the generation of ROIs and
whether antioxidants such as butylated hydroxyanisole (BHA), vitamin E,
and catalase might inhibit the hypertrophy in cultured
neonatal rat cardiac myocytes. ROIs were measured by the ROI-specific
probe 2',7'-dichlorofluorescin diacetate in cultured cardiac myocytes.
We demonstrated that TNF- and Ang II induced the generation of ROIs
in a dose-dependent manner. TNF- (10 ng/mL) and Ang II (100 nmol/L)
enlarged cardiac myocytes and increased [3H]leucine
uptake, and BHA (10 µmol/L) significantly inhibited both
effects. Other antioxidants, such as vitamin E (1 µg/mL) and catalase
(100 U/mL), also inhibited the enlargement of cardiac myocytes induced
by TNF-. and Ang II cause
hypertrophy in part via the generation of ROIs in cardiac
myocytes.
Key Words: myocytes • cells • hypertrophy • growth substances • antioxidants
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