Ischemic insult induced apoptotic changes in PC12 cells: protection by trans resveratrol

Eur J Pharmacol. 2011 Sep;666(1-3):5-11. doi: 10.1016/j.ejphar.2011.05.015. Epub 2011 May 23.


In this study, we determined the protective potential of trans resveratrol against oxygen-glucose deprivation (OGD) induced reactive oxygen species mediated apoptotic damages in PC12 cells. In vitro model of ischemic cerebral stroke was created by keeping cells in an OGD condition for 6h followed by 24h reoxygenation. Cells received biologically safe doses (5, 10, and 25 μM) of trans resveratrol in the following schedules for 24h prior to OGD; during 6h of OGD; for 24h post OGD and whole treatment group which starts from 24h before OGD and lasted to 24h post OGD. Anti-ischemic potential of trans resveratrol was assessed by measuring the regulation of lipid peroxidation, reactive oxygen species production, glutathione content, and expression (mRNA and protein) of apoptotic markers such as Bax, Bcl(2) and Caspase-3. Hypoxia inducible factor-1α (HIF-1α) was also assessed to correlate the changes with ischemic injuries. Significant (P<0.05) restoration in lipid peroxidation, reactive oxygen species, and glutathione content were observed following the treatment of trans resveratrol in cells receiving OGD and re-oxygenation. Changes induced by trans resveratrol could be correlated well with alterations in the expression of Bax, Bcl(2), Caspase-3 and HIF-1α. These results indicate that trans resveratrol administration attenuates free radical formation and mitochondria mediated apoptosis perhaps by regulating the expressions of Bax, Bcl(2,) and Caspase-3 in PC12 cells receiving OGD and re-oxygenation insult.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis / drug effects*
  • Apoptosis / genetics
  • Brain Ischemia / genetics
  • Brain Ischemia / metabolism
  • Brain Ischemia / pathology*
  • Brain Ischemia / prevention & control
  • Caspase 3 / biosynthesis
  • Caspase 3 / genetics
  • Glucose / metabolism
  • Glutathione / metabolism
  • Hypoxia-Inducible Factor 1, alpha Subunit / biosynthesis
  • Hypoxia-Inducible Factor 1, alpha Subunit / genetics
  • Lipid Peroxidation / drug effects
  • Neurons / drug effects
  • Neurons / metabolism
  • Neurons / pathology
  • Neuroprotective Agents / pharmacology*
  • Oxidative Stress / drug effects
  • Oxidative Stress / genetics
  • Oxygen / metabolism
  • PC12 Cells
  • Proto-Oncogene Proteins c-bcl-2 / biosynthesis
  • Proto-Oncogene Proteins c-bcl-2 / genetics
  • Rats
  • Reactive Oxygen Species / metabolism
  • Resveratrol
  • Stilbenes / pharmacology*
  • Transcription, Genetic / drug effects
  • bcl-2-Associated X Protein / biosynthesis
  • bcl-2-Associated X Protein / genetics


  • Hif1a protein, rat
  • Hypoxia-Inducible Factor 1, alpha Subunit
  • Neuroprotective Agents
  • Proto-Oncogene Proteins c-bcl-2
  • Reactive Oxygen Species
  • Stilbenes
  • bcl-2-Associated X Protein
  • Caspase 3
  • Glutathione
  • Glucose
  • Resveratrol
  • Oxygen