Neuroprotective Effects of p66^Shc Knock-out on Hypoxic-ischemic Brain Injury in Mice

  Objective  To explore neuroprotective effects of p66^Shc knock-out on hypoxic-ischemic brain injury in mice and possible underlining mechanisms.

  Methods  C57 mice were divided into 3 groups:sham-operation group (SO, wild type), hypoxic-ischemic wild type group (HIWT) and hypoxic-ischemic p66^Shc knock-out group (HIKO), 20 mice each group. HIBI model making:ligation of the right common carotid artery and then exposure to a hypoxic environment. The neurological dysfunction score, HIBI lesion volume, serum neuron specific enolase (NSE) level and interleukin (IL)-1β level in brain tissue were measured and compared.

  Results  Twenty-four hours after HIBI, the neurological function of HIKO mice was better than that of HIWT mice, the HIBI lesion volume of HIKO mice was smaller than that of HIWT mice, the serum NSE level of HIKO mice was much lower than that of HIWT mice, IL-1β level in the brain tissue of HIKO mice was much lower than that of HIWT mice (all P < 0.05).

  Conclusion  p66^Shc knock-out plays an important role in neuroprotective effects on HIBI of mice, possibly through attenuating IL-1β expression in the brain tissue after HIBI.