J4 ›› 2012, Vol. 38 ›› Issue (6): 1114-1118.

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Expression of neuroglobin in brain tissue of rats with cerebral infarction and its neuroprotective mechanisms

ZHANG Bei, LI Ya-jun, ZHANG Shi-jun, REN Hui-yun, WANG Min-juan, GUO Chang-jiang   

  1. Department of Neurology,Affiliated Hospital,Xi’[KG-*3]an Medical University,Xi’an 710077,China
  • Received:2012-07-26 Published:2012-11-28

Abstract:

Objective  To observe the expression of neuroglobin (Ngb)in brain tissue of rats with cerebral infarction and its effect on  PI3-K/Akt signaling pathway,and to study their effects on cerebral ischemic injury and  the possible mechanisms of the neuroprotective effect of Ngb.Methods  60 SD rats were randomly divided into  sham operation group,ischemia group,and Hemin group,LY group,and Hemin+LY group,and there were 12 rats in each group.Cerebral infarction models were established by middle cerebral artery thread embolism method.All rats were sacrificed 24 h after operation for neurological evaluation and detection of  cerebralinfarction volume, and the expression levels of Ngb and Akt mRNA were detected by RT-PCR.Results There was not any  area unstained by triphenyltetrazolium chloride and any neurologic impairment found in rats in sham operation group.Compared with ischemia group,the expression levels  of Ngb and Akt mRNA in Hemin group were increased significantly(P<0.01),with better neurological function(P<0.05) and less volume of cerebral infarction(P<0.01).The volume of cerebral infarction(P<0.01) and the neurological impairments (P<0.05)in LY group were increased,and the expression level of Akt mRNA  in LY group was lower(P<0.01)than that in ischemia group,and there was  no significant difference in the expression of  Ngb (P>0.05).The cerebral tissue damage in Hemin+LY group was aggrevated,and the expression level of Akt mRNA was decreased (P<0.01),while the level of Ngb mRNA was not inhibited by LY294002  (P>0.05) compared with Hemin group.Conclusion Ngb can reduce the voume of cerebral infarction and improve neurological function after focal cerebral ischemia in rats and its neuroprotective effect may be realized by activating PI3-K/Akt signaling pathway.

Key words:  neuroglobin;phosphoinositide-3 kinase/serine-threonine kinase;cerebral infarction

CLC Number: 

  • R743.33