| Objective To study the effect of on the c-fos expression in rats with cerebral ischemia reperfusion injury and to discuss its nerve protection mechanism., and to study the experimental evidence for the relationship between c-fos and neuronal apoptosis.Methods One hundred and ninty-eight healthy male Wistar rats were chosen to establish focal cerebral ischemia reperfusion models with middle cerebral artery thread embolism method and were randomly divided into sham operation group,ischemia/ reperfusion group, as well as ischemia and reperfusion treated with sodium aescinate group. The sham group had eighteen rats in it.The latter two were further divided into five subgroups according to reperfusion time interval of 6h,12h,24h,48h,72h after brain ischemia, with eighteen rats in each subgroup. Sodium aescinate treatment groups were given Sodium aescinate at dose of 5mg/kg/time, atfer 24h were given 5mg/kg/d,(drugs were dituted with NS to lml),the sham and ischemia/reperfusion groups were given the same dose of NS. To observe neurologic scores, infarct size, change of pathomorpHology and the c-fos expression in brain tissue was measured with immunohistochemical method image analysis.Results 1. Compared with the sham group, the ischemia/reperfusion group and sodium aescinate treatment group had different extent neurological deficit, but the ischemia/reperfusion group had improvement of neurological function in comparison with the ischemia/reperfusion group.2. The infarct volume of the ischemia/reperfusion and sodium aescinate treatment groups was obvious increased from 12h to 24h, it was little changed from 48h to 72h, and the sodium aescinate treatment group was all obviously smaller than the ischemia/ reperfusion group in the same time, (P<0.05); 3. Pathomorphology changes:The neurons in the sham group were unchanged. In the ischemia/reperfusion group there were obvious infarction. The cortex located the ischemia region of right brain were edematous significantly in the ischemia/reperfusion group; In the sodium aescinate treatment group there were also infarction, but the region of infarction were smaller than ischemia/reperfusion group, and cerebral edema and infiltration of neutropHil were light than the ischemia/reperfusion group.4. The expression of c-fos in ischemia/reperfusion and sodium aescinate treatment groups were obviously increased than the sham group. (P<0.05), moreover, it was started to increase at 6h after ischemia reperfusion, reached the peak at 24h, decreased in 48h, and reached the lowest on 72h in cerebral ischemia and reperfusion group. The expression of c-fos in the same time groups of the cerebral ischemia and reperfusion treated with sodium aescinate group all obviously decreased(P<0.05).Conclusion The c-fos expression may be one of the mechanism which induce neuronal apoptosis after cerebral ischemia and reperfusion,and sodium aescinate can help recovery of damaged brain by decreasing c-fos expression after early brain ischemia and reperfusion. |
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