Inhibitory effects of antioxidants on neonatal rat cardiac myocyte hypertrophy induced by tumor necrosis factor-α and angiotensin II

Kazufumi Nakamura*, Kazuo Fushimi, Hirosuke Kouchi, Koichiro Mihara, Masahiro Miyazaki, Tohru Ohe, Masayoshi Namba

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

413 Scopus citations

Abstract

Background - Tumor necrosis factor-α (TNF-α) 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-α and Ang II might cause myocyte hypertrophy via the generation of ROIs. Methods and Results - To test the hypothesis, we tested whether TNF-α 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-α and Ang II induced the generation of ROIS in a dose-dependent manner. TNF-α (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-α. Conclusions - These results indicate that TNF-α and Ang II cause hypertrophy in part via the generation of ROIs in cardiac myocytes.

Original languageEnglish (US)
Pages (from-to)794-799
Number of pages6
JournalCirculation
Volume98
Issue number8
DOIs
StatePublished - Aug 15 1998

Keywords

  • Antioxidants
  • Cells
  • Growth substances
  • Hypertrophy
  • Myocytes

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

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