| ObjectiveTo observe the expression of Bcl-2 and Bax in brain tissue of the middle cerebral artery occlusion/reperfusion (MCAO/R) model, when given Granulocyte-Colony Stimulating Factor (G-CSF) treatment. And to explore neuroprotective effect of G-CSF and its mechanism.MethodsThirty-six adult healthy male SD rats were randomly divided into sham-operated group,vehide group and G-CSF treatment group. (n=12). 6 rats in each group were randomly used for immunohistochemical staining and apoptosis determination. The others were used to measure the volume of cerebral infarction. Middle cerebral artery occlusion and reperfusion model was established by suture method in vehide group and G-CSF treatment group. The sham-operated group only received separating of artery, artery ligation and embolization were not received. Rats in G-CSF treatment group received subcutaneous injection of rhG-CSF (50μg/kg) immediately after reperfusion and 24h after reperfusion. Model + vehicle group rats were injected the same capacity of saline at the same time. Infarct volume was measured by triphenyltetrazolium chloride staining. TUNEL technique was carried out to detect the changes of apoptotic cells. The expression of bcl-2 and bax in brain tissues were measured by immunohistochemical methods and their gray value was measured by imaging analysis system.Results1 Neurological function score:the rats of vehicle group and G-CSF treatment group had certain degrees of neurological dysfunction. Compared with the vehide group, neurological function score was significantly lower in the G-CSF treatment group (P<0. 05).2 Determination of infarction volume: after stained by 2,3,5 - triphenyl tetrazolium chloride (TTC), some areas of rat brain were not stained in vehicle group and G-CSF treatment group. Compared with the vehide group, Infarction volume was significantly smaller in G-CSF treatment group (P<0. 05).3 Immunohistochemistry: the expression of bcl-2 and bax in vehicle group and G-CSF treatment group increased compared with the sham-operated group (P<0. 05). Compared with the vehide group, apoptotic cells were significantly decreased (P<0. 05), The expression of bax was significantly decreased (P<0. 05), the expression of bcl-2 was significantly increased (P<0. 05) in the G-CSF treatment group. Conclusion1 G-CSF therapy can reduce neurological function score;2 G-CSF therapy can reduce infarction volume of ischemia and reperfusion rats;3 G-CSF treatment may inhibit apoptosis of neurol cells caused by the ischemia-reperfusion injury and increase the expression of Bcl-2, and decrease the expression of Bax. This maybe one of the neuroprotective mechanism of G-CSF.
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