| Objective:This study to observe the brain ischemic postconditioning ofexpression of STAT3protein and alteration of apoptosis associated protein Caspase-3and thechanges of apoptosis cells after focal cerebral ischemia/reperfusion.The relation betweentyrosine phosphorylation of STAT3,the apoptosis associated protein Caspase-3and apoptosiscells were also investigated,in order to explore the mechanism of STAT3/Caspase-3signaltransduction pathway after cerebral ischemia/reperfusion,to participated in the regulation ofapoptosis,to find the brain protecting mechanism and looking for new targets and provide theguiding basis for changing clinical treatment programs.Methods:The middle cerebral arteryocclusion(MCAO) models were established by using the intraluminal suture occlusion methodin the right middle cerebral artery of SD rats. There are one hundred male SD rats with bodyweight between280g~300g randomly divided into three groups:sham-operation group(shamn=10), ischemia/reperfusion group(I/R n=45), ischemic postconditioning group(I/P n=45).Eachgroup was observed at six time point which were2h6h12h24h48h72h after the operation.And at each time point5rats were observed. And in the I/R group and the I/P group, every fiverats at the each time point of24h,48h and72h after ischemia2h were done TTC staining tomeasure the volume of cerebral infarction. Water content of brain tissue was detected by thedry-wet weight method at different time point.The nerve functional impairment and the modelssuccess criteria were judged by Neurological deficit score. The expressions change of STAT3 Caspase-3were detected by immunohistochemistry in different parts of rat brain tissue, andthe neuronal apoptosis in ischemia cerebral were evaluated by TUNEL assay.Result:1.Changesof the neurologic deficits score Neurologic deficits score of the I/R group at eachcorresponding time point which in2h72h after the operation was obviously lower than thesham group (P<0.05), neurologic deficits score of the I/P group at each corresponding timepoint which in12h72h was obviously higher than the I/R group (P<0.05).2.There were notthe expression of STAT3cells in tissue of normal control group and sham group. In ischemiazone including ischemia penumbra and ischemia core zone, the STAT3cells positive neuronsfirstly detected2hour after reperfusion, and reached peak at24hours, then it graduallydecreased. The expression of STAT3cells was obviously higher than the sham group at eachcorresponding time point (P0.05), and the expression of STAT3cells in tissue of the IPOgroup was obviously higher than the I/R group at each corresponding time point which in12h72h(P<0.05).3.The Caspase-3cells were occasionally observed in brain tissue in thesham group.The expression of Caspase-3cells was increased in ischemia penumbra zone afterfocal cerebral ischemia/reperfusion,the cells were lower than the ischemia core zone whichchanges of ischemia surrounding area.Compared with the sham group, the expression ofCaspase-3cells which in12h72h was increased obviously in cerebral I/R group(P0.05).The visible expression of a small amount of Caspase-3cells at2h after reperfusion,6h~12henhanced expression after reperfusion, and reached peak at24hours, then it graduallydecreased at72h. The expression of Caspase-3cells in tissue of the IPO group was obviouslylower than the I/R group at each corresponding time point which in12h72h(P<0.05),wasobviously higher than the sham group at each corresponding time point (P0.05).4.The amountof apoptosis cells reaches the peak after ischemia/reperfusion24~48hours models groups was obviously higher than the sham group (P0.05), and then it gradually decreased.5.Changes ofapoptotic cells and of STAT3Caspase-3cells expression consistent with thechange.Correlative analysis showed that STAT3Caspase-3cells were positive correlation withthe neuronal apoptosis witch TNUEL positive cells (P0.05).And positive correlation with eachother STAT3Caspase-3cells in the ischemia zone (P0.05).6.At the same point of time afterischemic, the score of neurological impairment, the infarct volume and the expression ofCaspase-3apoptotic cells were lower in postconditioning than these in ischemiagroup(P0.05); the expression of STAT3cells was higher than them in ischemiagroup(P0.05).Conclusion:1.Neurologic deficits,Water content of brain tissue and ischemicpathological changes of brain tissue were typically shown after ischemia/reperfusion.2.Upregulation of STAT3and Caspase-3cells after focal cerebral ischemia/reperfusion.3.The expression of Caspase-3cells was elevated after focal cerebral ischemia/reperfusion, itmight lead to apoptosis. and overexpression of STAT3might regulated the expression ofCaspase-3cells.4.Cerebral ischemic postconditioning can protect the brain against the injuryof severe ischemic. Ischemic postconditioning can improve the neurological function, reducebrain edema and the pathological damage and the cerebral infarction volume, which wasinjuryed after ischemia/reperfusion. The protection mechanism of the ischemicpostconditioning may be associated with the addition of STAT3to decrease of Caspase-3expression and inhibition of apoptosis. |
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