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Neural Regen Res. 2015 Sep;10(9):1471-6. doi: 10.4103/1673-5374.165519.

Cerebrospinal fluid from rats given hypoxic preconditioning protects neurons from oxygen-glucose deprivation-induced injury.

Neural regeneration research

Yan-Bo Zhang, Zheng-Dong Guo, Mei-Yi Li, Si-Jie Li, Jing-Zhong Niu, Ming-Feng Yang, Xun-Ming Ji, Guo-Wei Lv

Affiliations

  1. Department of Neurology, Affiliated Hospital of Taishan Medical University, Taian, Shandong Province, China.
  2. Department of Endocrinology, Affiliated Hospital of Taishan Medical University, Taian, Shandong Province, China.
  3. Department of Neurology, Shandong Taishan Chronic Disease Hospital, Taian, Shandong Province, China.
  4. Hypoxia Medical Institute, Xuanwu Hospital, Capital Medical University, Beijing, China.

PMID: 26604909 PMCID: PMC4625514 DOI: 10.4103/1673-5374.165519

Abstract

Hypoxic preconditioning activates endogenous mechanisms that protect against cerebral ischemic and hypoxic injury. To better understand these protective mechanisms, adult rats were housed in a hypoxic environment (8% O2/92% N2) for 3 hours, and then in a normal oxygen environment for 12 hours. Their cerebrospinal fluid was obtained to culture cortical neurons from newborn rats for 1 day, and then the neurons were exposed to oxygen-glucose deprivation for 1.5 hours. The cerebrospinal fluid from rats subjected to hypoxic preconditioning reduced oxygen-glucose deprivation-induced injury, increased survival rate, upregulated Bcl-2 expression and downregulated Bax expression in the cultured cortical neurons, compared with control. These results indicate that cerebrospinal fluid from rats given hypoxic preconditioning protects against oxygen-glucose deprivation-induced injury by affecting apoptosis-related protein expression in neurons from newborn rats.

Keywords: Bcl-2/Bax; apoptosis; cerebral cortex; cerebrospinal fluid; hypoxic preconditioning; nerve regeneration; neural regeneration; neurons; oxygen-glucose deprivation

References

  1. J Neuroinflammation. 2014 Jan 31;11:22 - PubMed
  2. Mol Neurobiol. 2005;31(1-3):255-71 - PubMed
  3. Int J Dev Neurosci. 2014 Oct;37:69-75 - PubMed
  4. Synapse. 2015 Jan;69(1):7-14 - PubMed
  5. Neuron. 2011 Mar 10;69(5):893-905 - PubMed
  6. Oncol Rep. 2015 Jan;33(1):304-10 - PubMed
  7. J Recept Signal Transduct Res. 2016;36(1):14-20 - PubMed
  8. Toxicol Mech Methods. 2014 Dec;24(9):688-96 - PubMed
  9. J Physiol Pharmacol. 2014 Feb;65(1):41-53 - PubMed
  10. J Ethnopharmacol. 2014 May 28;154(1):156-62 - PubMed
  11. Food Chem Toxicol. 2014 Jan;63:18-29 - PubMed
  12. Sheng Li Xue Bao. 2008 Apr 25;60(2):249-53 - PubMed
  13. PLoS One. 2014 Jul 17;9(7):e102056 - PubMed
  14. Asian Pac J Cancer Prev. 2014;15(20):8617-22 - PubMed
  15. BMC Psychiatry. 2014 Dec 04;14:349 - PubMed
  16. Psychiatry Res. 2013 Jul 30;213(1):56-62 - PubMed
  17. J Neurochem. 1998 Sep;71(3):1215-20 - PubMed
  18. Sheng Li Xue Bao. 2011 Dec 25;63(6):491-7 - PubMed
  19. J Neurol Sci. 2014 Dec 15;347(1-2):66-77 - PubMed
  20. Exp Ther Med. 2014 Apr;7(4):843-848 - PubMed
  21. Sheng Li Xue Bao. 2001 Aug;53(4):325-8 - PubMed
  22. Nat Rev Neurosci. 2006 Jun;7(6):437-48 - PubMed
  23. Clin Interv Aging. 2014 Mar 10;9:411-8 - PubMed
  24. Pediatr Res. 2014 Jul;76(1):46-53 - PubMed

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