Neural Regeneration Research ›› 2015, Vol. 10 ›› Issue (1): 153-158.doi: 10.4103/1673-5374.150725

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The pathways by which mild hypothermia inhibits neuronal apoptosis following ischemia/reperfusion injury

Chun Luo 1, 2, Su-yue Pan 1, *   

  1. 1 Department of Neurology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong Province, China
    2 Department of Neurology, Guangxi Minzu Hospital, Nanning, Guangxi Zhuang Autonomous Region, China
  • Received:2014-10-12 Online:2015-01-15 Published:2015-01-15
  • Contact: Su-yue Pan, pansuyue82@126.com.

Abstract:

Several studies have demonstrated that mild hypothermia exhibits a neuroprotective role and it can inhibit endothelial cell apoptosis following ischemia/reperfusion injury by decreasing casp-ase-3 expression. It is hypothesized that mild hypothermia exhibits neuroprotective effects on neurons exposed to ischemia/reperfusion condition produced by oxygen-glucose deprivation. Mild hypothermia significantly reduced the number of apoptotic neurons, decreased the expression of pro-apoptotic protein Bax and increased mitochondrial membrane potential, with the peak of anti-apoptotic effect appearing between 6 and 12 hours after the injury. These findings indicate that mild hypothermia inhibits neuronal apoptosis following ischemia/reperfusion injury by protecting the mitochondria and that the effective time window is 6–12 hours after ischemia/reperfusion injury.

Key words: nerve regeneration, mild hypothermia, oxygen-glucose deprivation, cell apoptosis, neurons, mitochondrial membrane potential, Bax, ischemia/reperfusion, neural regeneration