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Journal of Applied Clinical Pediatrics ; (24)1986.
Article in Chinese | WPRIM | ID: wpr-638402

ABSTRACT

Objective To explore the survival mechanism of hippocampal ne urons after damage of hypoxia-ischemia and reperfusion of brain.Methods Seven days old SD rats(n=56) were randomly divided into hypoxia-ischemia br a in iniury(HIBD) group and sham group.The HIBD and reperfusion model was establis hed.The flowing of blood was de tected by multicolor Doppler.The p-CREB(phosphorylated c-AMP response element bi nding protein)and c-Jun were immunohistochemically evaluated in hippocampus.Thi onin staining was used to observe the apoptosis.Results The expression of p-CREB reache d the peak at 3,24 h postreperfusion in the right hippocampus of HIBD group,and then decreased to the normal level on the 7th day.In contral group the same reg ions showed basic immn-noreactivity.While c-Jun reached the peak at 6 h postreperfusion,then with a slightly decrease at 24 h;and at 48 h the other peak appeared,then with a gradual decline .On the 7th day the mumber of positive cells were still significanthy more than control group(P0.05).The sham animal showed very few apoptosis cells in the regio ns of hippocampus.Conclusions The persistent activation of CREB in the hippocampus regulates,the expression of c-Jun through the signal transductions and is involved in the course of neuron s′ survival and repair during the period of post hypoxia-ischemia reperfusion.I t is very important for the protection of the pyramidal hippocampal neurons on t he damaged side,especially for the sensitive region CA1. J Appl Clin Pediatr,2005,20(2):133-135

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