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Protective effect of calceolarioside on adriamycin-induced cardiomyocyte toxicity

  • Do Sung Kim
  • , Hyung Ryong Kim
  • , Eun Rhan Woo
  • , Dae Young Kwon
  • , Myung Sunny Kim
  • , Soo Wan Chae*
  • , Han Jung Chae
  • *Corresponding author for this work
  • School of Medicine
  • School of Dentistry
  • Chosun University
  • Korea Food Research Institute

Research output: Contribution to journalJournal articlepeer-review

Abstract

Adriamycin is a potent antitumor drug that is known to cause severe cardiotoxicity. This study examined the protective effect of calceolarioside on adriamycin-induced cardiomyocyte toxicity. Calceolarioside significantly inhibited the adriamycin induced cell death and caspase-3 activation, which may be explained by the increase in Bcl-2 expression and the inhibition of Bax expression. Calceolarioside increased the expression of the antioxidant molecules and decreased the level of intracellular reactive oxygen species. Catalase, glutathione, N-acetylcysteine, Mannitol and Mn-TBAP (manganese (III) tetrakis-(4-benzoic acid) porphyrin) significantly inhibited the H9c2 cell death induced by adriamycin. Calceolarioside significantly inhibited H9c2 cell death, and was more effective than that observed with the other antioxidants, including probucol, ascorbic acid, and alpha-tocopherol. Overall, these results suggest that calceolarioside can inhibit adriamycin-induced apoptosis in H9c2 cardiomyocyte by inhibiting the generation of reactive oxygen species. Calceolarioside may be a potential candidate agent that inhibits cardiomyocyte-toxicity in adriamycin-exposed patients.

Original languageEnglish
Pages (from-to)24-32
Number of pages9
JournalEuropean Journal of Pharmacology
Volume541
Issue number1-2
DOIs
StatePublished - 2006.07.10

Keywords

  • Adriamycin
  • Apoptosis
  • Calceolarioside
  • Reactive oxygen species

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