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Evid Based Complement Alternat Med. 2013;2013:716730. doi: 10.1155/2013/716730. Epub 2013 Jul 07.

Protective Effect of Punica granatum L. against Serum/Glucose Deprivation-Induced PC12 Cells Injury.

Evidence-based complementary and alternative medicine : eCAM

Fatemeh Forouzanfar, Amir Afkhami Goli, Elham Asadpour, Ahmad Ghorbani, Hamid Reza Sadeghnia

Affiliations

  1. Pharmacological Research Center of Medicinal Plants, Department of Pharmacology, School of Medicine, Mashhad University of Medical Sciences, Mashhad 917794-8564, Iran ; School of Veterinary Medicine, Ferdowsi University of Mashhad, Mashhad, Iran.

PMID: 23935674 PMCID: PMC3723082 DOI: 10.1155/2013/716730

Abstract

The discovery and development of natural products with potent antioxidant, anti-inflammatory, and antiapoptotic properties have been one of the most interesting and promising approaches in the search for the treatment of many neurodegenerative diseases including ischemic stroke. Serum/glucose deprivation (SGD) has served as an excellent in vitro model for the understanding of the molecular mechanisms of neuronal damage during ischemia and for the development of neuroprotective drugs against ischemia-induced brain injury. Recent studies suggested that pomegranate (Punica granatum L.) or its active constituents exert pharmacological actions such as antioxidant, anti-inflammatory, and neuroprotective properties. Therefore, in this study we investigated the possible protective effects of different extracts of pomegranate against SGD-induced PC12 cells injury. Initially, the cells were pretreated with different concentrations of pulp hydroalcoholic extract (PHE), pulp aqueous extract (PAE) and pomegranate juice (PJ) for 2 h and then deprived of serum/glucose (SGD) for 6 and 12 h. SGD caused a significant reduction in cell viability (measured by the MTT assay) after 6 and 12 h, as compared with control cells (P < 0.001). Pretreatment with PHE, PAE, and PJ significantly and concentration-dependently increased cell viability following SGD insult for 6 and 12 h. A significant increase in DNA damage (measured by the comet assay) was seen in nuclei of cells following SGD for 12 h (P < 0.001). In control groups, no significant difference was seen in DNA damage between PHE, PAE, and PJ-pretreated and vehicle-pretreated PC12 cells (P > 0.05). PHE, PAE, and PJ pretreatment resulted in a significant decrease in DNA damage following ischemic insult (P < 0.001). This suppression of DNA damage by PHE, PAE and PJ was found to be concentration dependent. These data indicate that there is a cytoprotective property in PHE, PAE, and PJ under SGD condition in PC12 cells, suggesting that pomegranate has the potential to be used as a new therapeutic strategy for neurodegenerative disorders.

References

  1. J Inflamm (Lond). 2009 Jan 08;6:1 - PubMed
  2. Folia Neuropathol. 2011;49(2):78-87 - PubMed
  3. Carcinogenesis. 2011 Jun;32(6):888-96 - PubMed
  4. Foodborne Pathog Dis. 2010 Dec;7(12):1473-9 - PubMed
  5. Photochem Photobiol. 2010 Nov-Dec;86(6):1318-26 - PubMed
  6. Int Rev Neurobiol. 2009;85:363-74 - PubMed
  7. DNA Cell Biol. 2008 Dec;27(12):657-64 - PubMed
  8. Atherosclerosis. 2007 Dec;195(2):313-21 - PubMed
  9. Int J Oncol. 2003 Sep;23(3):705-12 - PubMed
  10. Acta Physiol Hung. 2011 Dec;98(4):409-20 - PubMed
  11. J Agric Food Chem. 2007 Nov 14;55(23):9559-70 - PubMed
  12. Pharmacogn Mag. 2011 Apr;7(26):161-4 - PubMed
  13. Pediatr Res. 2005 Jun;57(6):858-64 - PubMed
  14. J Agric Food Chem. 2011 Apr 27;59(8):4225-31 - PubMed
  15. J Nutr Biochem. 2004 Jan;15(1):2-11 - PubMed
  16. Avicenna J Phytomed. 2012 Summer;2(3):125-32 - PubMed
  17. Phytother Res. 2009 Nov;23(11):1565-74 - PubMed
  18. Atherosclerosis. 2006 Aug;187(2):363-71 - PubMed
  19. J Med Food. 2011 Dec;14(12):1638-46 - PubMed
  20. J Food Sci. 2010 Sep;75(7):C626-32 - PubMed
  21. J Med Food. 2011 Jul-Aug;14(7-8):695-701 - PubMed
  22. Neurobiol Dis. 2006 Dec;24(3):506-15 - PubMed
  23. J Int Acad Periodontol. 2005 Jul;7(3):70-9 - PubMed
  24. J Immunol Methods. 1983 Dec 16;65(1-2):55-63 - PubMed
  25. Evid Based Complement Alternat Med. 2012;2012:382763 - PubMed
  26. Cell Mol Neurobiol. 2010 May;30(4):591-8 - PubMed
  27. Mol Biotechnol. 2007 Sep;37(1):52-7 - PubMed
  28. J Cereb Blood Flow Metab. 2005 Feb;25(2):154-162 - PubMed
  29. Antioxid Redox Signal. 2012 Dec 1;17(11):1610-55 - PubMed
  30. Evid Based Complement Alternat Med. 2012;2012:147202 - PubMed
  31. Z Lebensm Unters Forsch. 1996 Oct;203(4):374-8 - PubMed
  32. Dev Neurosci. 2007;29(4-5):363-72 - PubMed
  33. J Food Sci. 2011 Jun-Jul;76(5):C707-13 - PubMed
  34. J Food Sci. 2011 Aug;76(6):C795-800 - PubMed
  35. J Nutr Biochem. 2005 Jun;16(6):360-7 - PubMed
  36. J Agric Food Chem. 2000 Oct;48(10):4581-9 - PubMed
  37. J Neuroendocrinol. 2009 Oct;21(10):841-9 - PubMed
  38. Evid Based Complement Alternat Med. 2013;2013:371813 - PubMed
  39. Brain Res. 2008 Nov 6;1239:24-35 - PubMed
  40. Evid Based Complement Alternat Med. 2013;2013:789764 - PubMed
  41. J Agric Food Chem. 2008 Feb 13;56(3):1148-57 - PubMed
  42. Drugs Exp Clin Res. 2002;28(2-3):49-62 - PubMed
  43. Neurochem Int. 2004 Oct;45(5):619-26 - PubMed
  44. Anticancer Res. 2005 Mar-Apr;25(2A):971-9 - PubMed
  45. Naunyn Schmiedebergs Arch Pharmacol. 2002 Jun;365(6):434-41 - PubMed
  46. Isr Med Assoc J. 2011 Aug;13(8):474-9 - PubMed
  47. Nitric Oxide. 2006 Nov;15(3):259-63 - PubMed
  48. Circulation. 2007 Feb 6;115(5):e69-171 - PubMed
  49. Food Chem Toxicol. 2006 Jul;44(7):984-93 - PubMed
  50. Fitoterapia. 2005 Mar;76(2):181-6 - PubMed
  51. Biochemistry (Mosc). 2004 Jan;69(1):75-80, 1 p preceding 75 - PubMed
  52. Blood. 2011 Jan 27;117(4):1311-4 - PubMed
  53. Carcinogenesis. 2006 Jul;27(7):1445-53 - PubMed
  54. Evid Based Complement Alternat Med. 2013;2013:247504 - PubMed
  55. Evid Based Complement Alternat Med. 2013;2013:247145 - PubMed

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