Expression of P-P38 in hippocampus CA1 region of bcl-2 transgenic rats after global cerebral ischemia reperfusion

Objective To investigate the expression of P-P38 in hippocampus CA1 region of bcl-2 transgenic rats after global cerebral ischemia reperfusion.Methods Ninety healthy male SD rats were randomly divided into sham operation group(SO group,n=30),ischemia reperfusion group(IR group,n=30)and bcl-2 transgenic group(bcl-2 group,n=30).Blood vessels of rats in SO group were just exposed but not occluded;the rats were induced to establish the global cerebral i schemia/reperfusion model by 4-VO method;the rats in bcl-2 group were performed as the same as IR group after establishment of the bcl-2 transgenic model.The rats were executed at 2,6,12,24,48,72 h after reperfusion,respectively.The neuronal morphology,cell apoptosis and the expression of P-P38 in hippocampus CA1 gyrus were examined by HE staining,TUNEL staining and immunohistochemical staining method.Results HE staining showed that the neuron in CA1 region in IR group decreased at 48 h after global cerebral ischemia reperfusion,companying with neuron disarrangement,nucleus membrane indistinction and nucleolus disappearance,however,no obvious changes were found in bcl-2 group.Immunohistochemical staining showed P-P38was negative in SO group,and expressed weakly in CA1 in IR group at 2 h after global cerebral ischemia reperfusion,then peaked at 48 h.Expression of P-P38 at each time point in bcl-2 group was significantly weaker than that in IR group(P0.05),although the expression trend in bcl-2 group was similar to that in IR group.TUNEL staining showed that only few apoptosis cells were found in SO group,while the positive apoptosis cells reached the peak at 48 h after global cerebral ischemia reperfusion in CA1 region of hippocampus in IR group.The positive number of apoptosis cell at 12 h,24 h,48 h,72 h after global cerebral ischemia reperfusion in bcl-2 group was much less than that in IR group(P0.05).Conclusion P-P38 expression increases in hippocampus CA1 region after global ischemia reperfusion,but bcl-2 could inhibit the neuron apoptosis through suppressing the expression of P-P38.