Influence Of 2DG On Neuron Apoptosis And Unification Of ER And Mitochondrium On Neuron Apoptosis In Fetal Distress Rat

Objective : The present study was undertaken to evaluate the unification of ER and mitochondrium on neuron apoptosis in fetal distress rat. We also investigated the influence and the protective role of 2-deoxyglucose, which is a inducer of GRP78.Methods :Establish intrauterus distress model with SD pregnant (17day)rat,the pregnant rats were divided into three group:normal group ,ischemia-reperfusion group which was divided into reperfusion3h,6h,12h,24h and 2-deoxyglucose treatment group which was divided into reperfusion3h,6h,12h,24h. To detect neuron apoptosis by He staining and TUNEL staining and observe the cerebral pathological changes,and observing the influence of 2- deoxyglucose on neuron apoptosis. To extract brain tissue protein and detect the expression of GRP78,caspase-9,-12,and cytoron C protein by Western blot technique. To observe the relationship of thoseprotein and neuron apoptosis,and observing the influence of 2- deoxyglucose on those protein. Results :(1)The brain of fetal rat,which experienced hypoxia- ischemia-reperfusion damage in uterus,occurred various degree damage and apoptosis. With the progression of reperfusion,the number of the apoptotic cell became much more abundant(P﹤0.05),the maximal levels of neuron apoptosis was attained at reperfusion 24h. (2) the expression of GRP78,caspase-9,-12,and cytoron C protein was minimal levels on normal group. (3)GRP78,caspase-9,-12,cytoron C protein levels increase in ischemia-reperfusion group(P﹤0.05). With the progression of reperfusion,GRP78 protein levels became reducing,but caspase-9,-12,cytoron C protein levels became incrasing,the maximal levels was attained at reperfusion 12h. (4) GRP78 protein levels obviously increase in 2-deoxyglucose treatment group to contrast normal group(P﹤0.05),the maximal levels was attained at reperfusion 12h ,but caspase-9,-12 ,cytoron C protein levels obviously reduce(P﹤0.05).Conclusion :The brain of fetal rat,which experienced hypoxia- ischemia-reperfusion damage in uterus,occurred various degree damage and apoptosis,the result caused by unification of ER and mitochondrium. 2-deoxyglucose raise GRP78 expression,and decrease caspase-9,-12 ,cytoron C protein levels,which degrade neuron apoptosis.