Apurinic/apyrimidinic endonuclease 1 (APE1) contributes to resveratrol‑induced neuroprotection against oxygen‑glucose deprivation and re‑oxygenation injury in HT22 cells: Involvement in reducing oxidative DNA damage

  • Authors:
    • Jiao‑Ying Jia
    • Zhi‑Gang Tan
    • Min Liu
    • Yu‑Gang Jiang
  • View Affiliations

  • Published online on: October 17, 2017     https://doi.org/10.3892/mmr.2017.7799
  • Pages: 9786-9794
Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )


Abstract

Resveratrol, a naturally occurring polyphenolic compound, exhibits a neuroprotective role in models of central nervous system diseases, including cerebral ischemia/reperfusion injury. Apurinic/apyrimidinic endonuclease 1 (APE1) is a multifunctional enzyme that contributes to base excision repair of oxidative DNA damage and redox activation of transcription factors, associated with neuronal survival against hypoxic‑ischemic injury. It was hypothesized that resveratrol protects HT22 cells against oxygen‑glucose deprivation and re‑oxygenation (OGD/R)‑induced injuries through upregulation of APE1. It was demonstrated that resveratrol pretreatment significantly increased the viability of HT22 cells and decreased the release of lactate dehydrogenase (LDH), accompanied by the upregulation of APE1 mRNA, and protein levels, as well as the activity of APE1 under OGD/R conditions. In addition, resveratrol reversed OGD/R‑induced oxidative DNA damage as evidenced by the decreases in the levels of 8‑hydroxy‑2'‑deoxyguanosine and APE sites. However, APE1 knockdown using short hairpin RNA sequence targeting APE1 abolished resveratrol‑elicited beneficent effects against OGD/R‑induced cytotoxicity and oxidative stress. This was indicated by decreased cell viability, superoxide dismutase activity and glutathione levels, and increased LDH release and reactive oxygen species levels. The results of the present study indicate that APE1 contributes to the protective effects of resveratrol against neonatal hypoxic‑ischemic brain injuries, and suggest that DNA repair enzymes, including APE1, may be a unique strategy for neuroprotection against this disease.
View Figures
View References

Related Articles

Journal Cover

December-2017
Volume 16 Issue 6

Print ISSN: 1791-2997
Online ISSN:1791-3004

Sign up for eToc alerts

Recommend to Library

Copy and paste a formatted citation
x
Spandidos Publications style
Jia JY, Tan ZG, Liu M and Jiang YG: Apurinic/apyrimidinic endonuclease 1 (APE1) contributes to resveratrol‑induced neuroprotection against oxygen‑glucose deprivation and re‑oxygenation injury in HT22 cells: Involvement in reducing oxidative DNA damage. Mol Med Rep 16: 9786-9794, 2017
APA
Jia, J., Tan, Z., Liu, M., & Jiang, Y. (2017). Apurinic/apyrimidinic endonuclease 1 (APE1) contributes to resveratrol‑induced neuroprotection against oxygen‑glucose deprivation and re‑oxygenation injury in HT22 cells: Involvement in reducing oxidative DNA damage. Molecular Medicine Reports, 16, 9786-9794. https://doi.org/10.3892/mmr.2017.7799
MLA
Jia, J., Tan, Z., Liu, M., Jiang, Y."Apurinic/apyrimidinic endonuclease 1 (APE1) contributes to resveratrol‑induced neuroprotection against oxygen‑glucose deprivation and re‑oxygenation injury in HT22 cells: Involvement in reducing oxidative DNA damage". Molecular Medicine Reports 16.6 (2017): 9786-9794.
Chicago
Jia, J., Tan, Z., Liu, M., Jiang, Y."Apurinic/apyrimidinic endonuclease 1 (APE1) contributes to resveratrol‑induced neuroprotection against oxygen‑glucose deprivation and re‑oxygenation injury in HT22 cells: Involvement in reducing oxidative DNA damage". Molecular Medicine Reports 16, no. 6 (2017): 9786-9794. https://doi.org/10.3892/mmr.2017.7799