| Objective:To observe the changes of infarction volume,neuron morphous,neuron apoptosis and expression of Bcl-2,Bax in rat brain after chronic intermittent hypoxia (CIH) combining cerebral ischemia-reperfusion injury.And then to explore the injury mechanism of chronic intermitten hypoxia(CIH).Methods: Fifty-eight healthy male rats were fractionated randomly fivegroups: the control group,sham operation group,ischemia-reperfusion 24 hours group and two CIH combining cerebral ischemia- reperfusion groups, which were exposed tointermittent hypoxia for 4 weeks and 8 weeks respectively,and then tomake cerebral ischemia model successly.Ischemia group and CIH combining cerebralischemia-reperfusion group were fractionated measurin volume group and immunohistochemistry group again, reperfusion points were 24 hours after cerebral ischemia two hours. The morphology changes were observed by microscope and the expression of Bcl-2 and Bax protein were investigated by using immunohistochemistry techniques respectively,and terminal deoxynucleotidyl transferase mediated dUTP-biotin nick end labeling (TUNEL) staining and TTC staining were used to observe infarction volume which the focal cerebral ischemia was induced by the transient right MCAO in Sprague-Dawley rats.The behavior scales of neural function of cerebral ischemia-reperfusion injury(CI/RI)of the rats was used to evaluate the neural function.Results: TTC staining and the neuralfunction of the rats showed the infarction volume and The neuralfunction of the rats in CIH 8 weeks combining cerebral ischemia-reperfusion group was much bigger than orther groups (P<0.05). Compared with the cerebral ischemia- reperfusion group, the infarction volume of CIH 4 weeks combining cerebral ischemia- reperfusion group was no significantly different ( P﹥0.05 ) . TUNEL-positive cells were more apparent in the perifocal tissue and particularly in the inner border regions immediately adjacent to the ischemic core. Compared with orther groups, the number of apoptotic cells of CIH 8 weeks combining cerebral ischemia-reperfusion group was significantly different(P﹤0.01).However,there was no significantly different between CIH 4 weeks combining cerebral ischemia-reperfusion group and the cerebral ischemia- reperfusion group(P﹥0.05). We found that immunity-positive cells were more apparent in the perifocal tissue and particularly in the inner border regions immediately adjacent to the ischemic core. The Bax positive staining cells and Bcl-2/Bax ratio decreased at CIH 8 weeks combining cerebral ischemia-reperfusion group Compared with orther groups(P<0.05),but in CIH 8 weeks combining cerebral ischemia- reperfusion group Bcl-2 positive staining cells were more than other group(P<0.01). The Bcl-2 positive staining cells and Bcl-2/Bax ratio of CIH 4 weeks combining cerebral ischemia- reperfusion group were less than cerebral ischemia- reperfusion group(P<0.01). However,there was no significantly different between the Bax positive staining cells of CIH 4 weeks combining cerebral ischemia-reperfusion group and that of the cerebral ischemia- reperfusion group(P﹥0.05). Compared with CIH 4 weeks combining cerebral ischemia-reperfusion group,the Bax positive staining cells,Bcl-2/Bax ratio and Bcl-2 positive staining cells in CIH 8 weeks combining cerebral ischemia-reperfusion group was no significantly different(P<0.05).Conclusions:These results indicated that that CIH could significantly increase the cerebral ischemia-reperfusion injury.It could increase the infarction volume and rats neural function. The numble increase of the apoptotic cells and the expression increase of Bax protein and decrease of Bcl-2 protein and Bcl-2/Bax ratio after cerebral ischemia-reperfusion injury could be induced by chronic intermittent hypoxia (CIH).The change of Bcl-2/Bax ratio would play a possible role regulating the neuronal survival or death during cerebral ischemia-reperfusion injury after chronic intermittent hypoxia (CIH).
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