| Objectives： The focal cerebral ischemia models made by rats to evaluate theneuroprotection of ischemic postconditioning(IPC) on ischemia/reperfusion(I/R) injuryin rats;to detect the associate protein expression levels of endoplasmic reticulumstress;to investigate the neuroprotection mechanisms of IPC.Methods：84male SD (weighted250-350g) rats were randomly assigned to7groups(n=12each):sham operated groups,I/R groups and IPC groups with different timeof reperfusion(3h,6h,12h).The rat models of the left middle cerebral arteryocclusion(MCAO) was established by suture-occluded method. I/R groups wererestored reperfusion for3h,6h,12h after MCAO for60min. IPC groups were given3cycles of30s reperfusion and10s occlusion after MCAO60min,and then allowedreperfusion for3h,6h,12h.Followed by3h,6h,12hof reperfusion all rats performedneurological deficit score (NDS)by Bederson6ranks5points scoring system.Taken6rats randomly from each group,the infarction volume was calculated by2,3,5-triphenyl-2H-tetrazolium chloride(TTC).Observed ischemic hippocampus CA1region neurons in morphological change by Hematoxylin-Eosin staining(HE)staining.The number of neuron apoptosis was examined by Terminal deoxynucleotidyltransferase mediated Biotin-dUTP niek-end labeling(TUNEL).The expression level ofGRP78and CHOP were detected by immunohistochemistry (IHC).Results：1.NDS and the percentage of cerebral infarct volume:there were noneurological dysfunction and cerebral infarction in rats in sham groups,rats in I/R andIPC groups showed neurological dysfunction and cerebral infarction vary.Comparedwith I/R groups,rats in IPC3h,6h groups decreased the NDS and reduced the infarctionsignificantly(p＜0.05).Compared with I/R3h group,rats in IPC3h group moresignificantly reduced the volume of infarction（p＜0.01）.2.HE staining: The neuronal in rats in sham group under by microscope preserved normal outline, round nuclei,prominent nucleli,there was no interspace between neurons and its surrounding tissue.Rats in I/R groups were observed typical ischemic change,hippocampus by HE staining,layers were shown more thinner, neurons and glial cells were decreased, edema,vacuolar degenerated,nucleus condensated, nucleoli disappeared,the margin betweenlesion area and its surrounding area could be seen clearly.3.TUNEL:Rats in sham groupshowed occasionally apoptotic cells.Rats in I/R and IPC groups showed apoptotic cellsvary.Compared with I/R groups,rats in IPC groups were do decrease AI in hippocampusCA1region（p＜0.05）.Compared with I/R3h group,rats in IPC3h group were moresignificantly reduced the A（Ip＜0.01）.4.IHC:(1) The mean optical density(MOD)valueof GRP78expression:Rats in sham group seldom expressed.Compared with shamgroup,the MOD value of GRP78expression were increased in I/R and IPC groups（p＜0.01）.Compared with I/R groups,the MOD value of GRP78expression in IPC groupswere significantly increased(p＜0.05).(2) The MOD value of CHOP expression:Rats insham group seldom expressed.Compared with sham group,the MOD value of CHOPexpression were increased in I/R and IPC groups（p＜0.01）.Compared with I/Rgroups,the MOD value of CHOP expression in IPC groups were significantlydecreased(p＜0.05).5.The correlation analysis of neuronal AI in ischemic hippocampusCA1region and the MOD value of GRP78、CHOP expression:The MOD value ofGRP78and neuronal AI were negative correlation（r=-0.930,p＜0.01）, the MOD valueof CHOP and neuronal AI were positive correlation（r=0.994,p＜0.01）.Conclusions: IPC can reduce the infarction volume,provide neuroprotectiveeffects.Inhibit the expression level of CHOP apoptosis molecule.stimulate theexpression level of GRP78.Suppress apoptosis reduced by ERS,relieve cerebral I/Rinjury,enhance neuroprotection. |
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