Display options
Share it on

Evid Based Complement Alternat Med. 2013;2013:802784. doi: 10.1155/2013/802784. Epub 2013 Oct 10.

BNC Protects H9c2 Cardiomyoblasts from H 2 O 2 -Induced Oxidative Injury through ERK1/2 Signaling Pathway.

Evidence-based complementary and alternative medicine : eCAM

Fangbo Zhang, Bin Huang, Ye Zhao, Shihuan Tang, Haiyu Xu, Lan Wang, Rixin Liang, Hongjun Yang

Affiliations

  1. Institute of Chinese Materia Medica, China Academy of Chinese Medical Sciences, Beijing 100700, China.

PMID: 24223618 PMCID: PMC3810482 DOI: 10.1155/2013/802784

Abstract

Buchang naoxintong capsule (BNC) is a traditional Chinese medicine approved for the treatment of cerebrovascular and cardiovascular diseases. However, little is known about the specific protective function or mechanism by which BNC protects against myocardial injury. This research was designed to investigate the cardioprotective effects of BNC in vitro model of hydrogen peroxide (H2O2)-induced H9c2 rat cardiomyoblasts. BNC intestinal absorption liquid was used in this study instead of drug-containing serum or extracting solution. Our study revealed that BNC preconditioning enhanced antioxidant function by increasing the activities of total-antioxygen capacity, total-superoxide dismutase, and catalase and by decreasing the production of reactive oxygen species and malondialdehyde. BNC preconditioning also activated extracellular signal-regulated kinases (ERK1/2) and inhibited apoptosis-related proteins such as poly ADP-ribose polymerase (PARP) and caspase-3. Additionally, preincubation with BNC reduced intracellular Ca(2+) concentration, improved mitochondrial membrane potential, and decreased the apoptosis rate of H9c2 cells in a dose-dependent manner. These data demonstrated that BNC protects H9c2 cardiomyoblasts from H2O2-induced oxidative injury by increasing antioxidant abilities, activating ERK1/2, and blocking Ca(2+)-dependent and mitochondria-mediated apoptosis. Based on our results, the potency of BNC for protecting H9c2 cells from oxidative damage is comparable to that of trimetazidine.

References

  1. Circ J. 2009 Mar;73(3):411-8 - PubMed
  2. Curr Opin Cell Biol. 1999 Apr;11(2):211-8 - PubMed
  3. J Hypertens. 2000 Jun;18(6):655-73 - PubMed
  4. Am J Cardiol. 2006 Sep 4;98(5A):8J-13J - PubMed
  5. Free Radic Biol Med. 2006 Jun 15;40(12):2206-13 - PubMed
  6. Cardiovasc Res. 2000 Aug 18;47(3):446-56 - PubMed
  7. J Mol Cell Cardiol. 2013 Jun;59:41-54 - PubMed
  8. J Mol Cell Cardiol. 2012 Jan;52(1):48-61 - PubMed
  9. J Cell Biochem. 2001;82(4):674-82 - PubMed
  10. Antioxid Redox Signal. 2011 Apr 15;14(8):1437-48 - PubMed
  11. J Clin Invest. 1997 Oct 1;100(7):1813-21 - PubMed
  12. Physiol Rev. 2008 Apr;88(2):581-609 - PubMed
  13. Evid Based Complement Alternat Med. 2012;2012:430262 - PubMed
  14. Am J Med. 1991 Sep 30;91(3C):14S-22S - PubMed
  15. Brain Res. 2004 Jan 16;996(1):55-66 - PubMed
  16. Apoptosis. 2000 Nov;5(5):415-8 - PubMed
  17. Evid Based Complement Alternat Med. 2011;2011:207034 - PubMed
  18. J Pharmacol Exp Ther. 2006 Jun;317(3):921-8 - PubMed
  19. J Biol Chem. 1999 Feb 19;274(8):5038-46 - PubMed
  20. J Ethnopharmacol. 2010 Jul 6;130(1):98-102 - PubMed
  21. Pharmacol Ther. 2001 Jan;89(1):29-46 - PubMed
  22. J Pharm Pharmacol. 2013 May;65(5):621-33 - PubMed
  23. Antioxid Redox Signal. 2006 Nov-Dec;8(11-12):2111-24 - PubMed
  24. Anesth Analg. 2005 Nov;101(5):1275-1287 - PubMed
  25. Circ Res. 2004 Nov 12;95(10):957-70 - PubMed
  26. J Pharmacol Exp Ther. 2009 May;329(2):543-50 - PubMed
  27. J Clin Invest. 1998 Jul 1;102(1):165-75 - PubMed
  28. Cardiovasc Res. 2009 Feb 15;81(3):465-73 - PubMed
  29. Curr Pharm Des. 2013;19(33):5891-6 - PubMed
  30. Molecules. 2011 Nov 17;16(11):9600-10 - PubMed
  31. Microbiol Mol Biol Rev. 2004 Jun;68(2):320-44 - PubMed

Publication Types