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Modulation of gene-expression profiles associated with sodium arsenite-induced cardiotoxicity by p-coumaric acid, a common dietary polyphenol.

Abstract
In the present study, the purpose was to investigate the effect of p-coumaric acid on the mRNA-expression levels of inflammatory cytokines, transcription factor, MAP kinases, and apoptotic proteins by real time reverse transcription polymerase chain reaction in the cardiac tissue of sodium arsenite exposed rats. Sodium arsenite administration (5 mg/kg/b.wt, once daily for 30 days) upregulated the mRNA-expression levels of inflammatory cytokines (interleukin-1 beta, interleukin-6, tumor necrosis factor-alpha, and tumor growth factor-beta), transcription factor (NF-Kb-Rel A), protein kinases (Janus kinase and p38), caspase 3, and proapoptotic protein Bax in the cardiac tissue of rats, but the antiapoptotic protein Bcl-2 mRNA expression was found be downregulated. However, p-coumaric acid (75, 100 mg/kg/b. wt. oral) pretreatment daily before the sodium arsenite exposure protected the changes in the above mRNA-expression profiles observed in the cardiac tissues. In conclusion, this study confirmed that p-coumaric acid could be a promising dietary agent for protecting against the sodium arsenite-induced cardiotoxicity.
AuthorsNagalakshmi Prasanna, Mahaboobkhan Rasool
JournalJournal of biochemical and molecular toxicology (J Biochem Mol Toxicol) Vol. 28 Issue 4 Pg. 174-80 (Apr 2014) ISSN: 1099-0461 [Electronic] United States
PMID24497207 (Publication Type: Journal Article)
Copyright© 2014 Wiley Periodicals, Inc.
Chemical References
  • Apoptosis Regulatory Proteins
  • Arsenites
  • Cardiotonic Agents
  • Coumaric Acids
  • Cytokines
  • Environmental Pollutants
  • Rela protein, rat
  • Sodium Compounds
  • Transcription Factor RelA
  • sodium arsenite
Topics
  • Animals
  • Apoptosis Regulatory Proteins (genetics, metabolism)
  • Arsenites (toxicity)
  • Cardiotonic Agents (pharmacology)
  • Coumaric Acids (pharmacology)
  • Cytokines (genetics, metabolism)
  • Environmental Pollutants (toxicity)
  • Gene Expression Regulation (drug effects)
  • Male
  • Myocardium (metabolism)
  • Rats, Wistar
  • Sodium Compounds (toxicity)
  • Transcription Factor RelA (genetics, metabolism)
  • Transcriptome (drug effects)

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