| Background and purpose:Ischemic cerebrolvascular disease is one of the common and frequently-occurring disease to life and health of the aged in nowadays.During the cerebral ischemia,the neurons died and caused homologous functional disorder. In the acute stage of cerebral ischemia,the neurons which located in the center of ischemia was necrotic.But the peripheral neurons was secondum death,that was apoptosis.Autogene expressed,followed with apoptosis.These gene controlled the apoptosis through intervened the process of apoptosis.The relationship was very intimate between the apoptosis related gene.The Bcl-2 can against ischemia and protecte the neurons. Our study through the model of focal cerebral ischemia/reperfusion in rats dealed with NGF,to observe the express of Bcl-2,Bax and VEGF. The aim is to investigate the neuroprotective mechanism of NGF for focal cerebral ischemia in rats.Methods: The 60 rats are radomly divided into four groups:normal control,sham operation(n=18),ischemic group(n=18),NGF treated group(n=18).Established the rat middle cerebral artery occlusion (MCAO) model with feformed Zea Longa suture occlusion and then the rats were evaluated with Zea Longa measuring scale,the model is thought to be successful if its score exceed one (including one score). The time of observation is 90 minute after ischemia and 24h,48h,72h after reperfusion.The treated group was intraperitoneal injected with NGF 1.0ml(500u/ml,Wuhan haite) at the reperfusion moment ,24h and 48h after reperfusion respectively.The Sham group and ischemic group was given with the same volume normal sodium at the same time and in the same ways.After refusion24h,48h,72h,every experimental animal was perfused with paraformaldehyde,taken brain,paraffin imbedding and section,then HE dyeing and immunohisto-chemistry detected.To observe the expression of Bcl-2,Bax,VEGFand pathological change of the neurons.Result: Ischemic damage is mainly restrict at ipsilateral frontal lobe,parietal cortex and dorsal caudate putamen.Middle cerebral artery(MCA) provides blood for them.The hippocamp was also damaged in some experimental rats.Comparing with ischemic group,the rats in NGF treated group neurologic impairment was not serious. In the cores of ischemic damage,neuron dyeing is very light,the amount of neuron decrease,cellular swelling,nuclear fragmentation,vascular was dilarationed around the core area ,with the time passed,core area's neuron loss was more noticeble.We can find the same pathologic change in the NGF treated group ,but the damage was less serious than ischemic group at the corresponding time.We can observe little Bcl-2,Bax positive cell,while Bcl-2,Bax positive cellcould obeserved in the ischemic group and NGF treated group's cerebral cortex,hippocampus. immunostaining positive cell is brown, cytoplasm and synapsis were dyed,cellular nucleus were not dyed.The mumber of Bcl-2 staining positive cells was increased obviousely in the NGF treated group(P<0.05).Bax staining positive cell number obviously decreased (P<0.05).Bcl-2/Bax ratio increase.In ischemic group and NGF treated group,the VEGF staining positive cells were significantly more than ischemic group.Conclusions:1.The model building of focal cerebral ischemia/reperfusion in rats is easy,safe,repetatus and pragmatic.It is the ideal animal model to study cerebral ischemia/reperfusion.2.It can lighten the pathological change through providing nerve growth factor post ischemia in rats.It tells us that NGF has the neuroprotective effect for ischemical reperfusion injury.3. The mechanism of neuroprotective effect of NGF maybe partly due to its effect of promoting Bcl-2 and VEGF,at the same time depressing the expression of Bax after cerebral ischemia reperfusion in rats.
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