Experimental Study On Ischemic Postconditioning On Ischemia Reperfusion Injury Of The Rats And The Change Impacts Of Bcl-2﹑GAP-43and Nogo-A

To use of intraluminal filament in rat brain ischemia/reperfusion model, using theischemic postconditioning (IP) to reduce the cerebral ischemia/reperfusion injury(I/R) and protective effect on nerve repair, delay reperfusion treatment time window. By detecting the expression of Bcl-2, GAP-43and Nogo-A protein to discuss the ischemic postconditioning is through the increase expression of Bcl-2,GAP-43and decrease of Nogo-A in ischemia-reperfusion of brain tissue play a protective role, and realize of IP delay reperfusion treatment time window, in order to verify the protective effect of IP on Ischemic cerebral infarction, seek new theoretical foundation for clinical guidance of the treatment and diagnosis of Ischemic cerebral infarction. Method1. To use of intraluminal filament in rat brainl/R model.20healthy adult maleSD rats were randomly divided into ischemia reperfusion for2h group and IP for4.5h group, each group of10; in focal cerebral I/R for24h give the neurological score; after24h give TTC staining for determinated the infarct volume.2.30healthy adult male SD rats were randomly divided into ischemia reperfusionfor2h group and IP for4.5h group, each group of15;after cerebral ischemia reperfusion for24hours take the brain tissue, Follow the steps of fixed, paraffin embedded and made the paraffin sections, Do HE staining, Apply immunohistochemical method and Western blot detect the expression levels of Nogo-A, GAP-43and Bcl-2. At last application the rank sum test, paired samples t-test statistical methods for data analysis and observation of pathological changes of brain tissue.Result(1) IP for4.5h group of infarct volume compared with ischemia reperfusion for2h were no significant differences.(2) IP for4.5h rats of the volume of cerebral infarction, neurological score for postoperative24h of Ludmila12points test, Zea Longa5points test and over hanging experiments compared with ischemia reperfusion2h group has no significant difference (P>0.05).(3)IP for4.5h of the changes of Nogo-A, GAP-43and Bcl-2was normal distribution, applying paired t-test, compared with ischemia reperfusion2h group was significant difference (P<0.05);Do slope experimental,the neurological score does not meet the normal distribution, using the Wilcoxon rank sum test, P=0.003<0.05, the two groups has significant difference.(4)IP for4.5h of the Western Blot result of Nogo-A,GAP-43and Bcl-2was normal distribution, but because of the different sample sizes, using independent samples t-test, compared with ischemia reperfusion2h group has significant difference (P<0.05).Conclusion(1) Ischemic postconditioning has cerebral protective effect, can extend the reperfusion time window to4.5h, for clinical ischemic cerebral stroke of thrombolytic therapy provides a new way of thinking.(2)IP for4.5h rats of the volume of cerebral infarction, neurological score for postoperative24h of Ludmila12points test, Zea Longa5points test and over hanging experiments compared with ischemia reperfusion2h group was no significant increase, explain IP can improve the neurological deficit.(3)IP for4.5h group of infarct volume compared with ischemia reperfusion for2h were no significant increase, the description of IP can reduce infarct volume caused by middle cerebral artery embolization.(4) IP can increase expression GAP-43and Bcl-2cerebral after ischemia reperfusion24h in infarct side of the basal ganglia, reduce expression of Nogo-A after cerebral ischemia reperfusion for24h in infarct side of the basal ganglia.(5) the group of IP of cerebral infarction in the side of the basal ganglia of GAP-43and Bcl-2positive cells and the Western Blot result compared with ischernia reperfusion for2h group increased significantly, the group of IP of cerebral infarction in the side of the basal ganglia of Nogo-A positive cells and the Western Blot result compared with ischemia reperfusion for2h group decreased largely, prompted IP can reduce the occurrence of cerebral ischemia neuronal apoptosis, to promote the regeneration of nerve, thus confirming that the inhibition of neuronal apoptosis may be a mechanism to play a cerebral protective effect of IP.