Sevoflurane Post-conditioning Enhanced Hippocampal Neuron Resistance to Global Cerebral Ischemia Induced by Cardiac Arrest in Rats through PI3K/Akt Survival Pathway

We investigated the relationship between the PI3K/Akt pathway and mitochondrial biogenesis and mitochondriaspecific antioxidant enzymes in sevoflurane-induced neuroprotection

Zhihua Wang; Zhi Ye; Guoqing Huang; Na Wang; E. Wang; Qulian Guo

2016

Scholarcy highlights

  • A brief period of global brain ischemia, such as that induced by cardiac arrest or cardiopulmonary bypass surgery can occur under various perioperative circumstances and result in long-term neurological disability or death
  • A continually improved outcome after global brain ischemia induced by CA or cardiopulmonary bypass surgery has been achieved in patients, there has been no revolutionary breakthrough
  • Growing evidence has shown that treatment with sevoflurane, a volatile anesthetic agent, before or after ischemia can improve neuronal recovery after the insult
  • Sevoflurane post-conditioning significantly attenuated the activation of caspase-3 and -9 to reduce post-ischemic neuronal apoptosis
  • Our data suggest that sevoflurane post-conditioning is remarkably effective in preventing neuronal apoptosis in the hippocampus in a model of CA-induced global cerebral ischemia
  • There were no significant differences in body weight, basal body temperature, breathing frequency, and heart rate of the rats among three groups
  • We have shown that sevoflurane post-conditioning triggered significant protection against CA-induced global cerebral ischemia by preserving mitochondrial biogenesis and promoting mitochondrial antioxidant enzymes, the underlying mechanism for sevoflurane’s neuroprotection effect remains to be elucidated
  • Administration of sevoflurane after reperfusion was able to significantly induce the gene and protein levels of mitochondrial pro-survival proteins, including PGC-1α, NRF1, and TFAM, up-regulate mitochondria-specific antioxidant enzyme expression, and restore mitochondrial integrity

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