The Effect Of NBP-pretreatment For HSP70 And TLR4 Expression Of Cerebral Ischemia-reperfusion Injury In Rats

Objective: To explore the effect of NBP-pretreatment on the histologic outcome,apoptosis at different time points on the model of focal cerebral ischemia-reperfusion injury inrats. To investigate the expresion of HSP70 and TLR4 in the model of focial cerebeal ischemiareperfusionand the effect of NBP-pretreatment.Methods:1. Seventy-two male adult Wistar rats were divided into sham operation group,ischemia-reperfusion group and NBP-pretreatment group randomly,reperfusion 6,12,24,48h foursub-groups were divided in each group according to their reperfused time point. 2. Focal cerebralischemia-reperfusion model was established by the occlusion of right middle cerebral artery. 3.HE staining of pathological changes in brain tissue morphology;neuronal apoptosis was detectedby TUNEL,to observe HSP70 and TLR4 expresion was by immunohistochemisery.Results: 1.HE staining shows that infarction and neuronal injury was relieved at differenttime points in the NBP-pretreatment group compared with I-R group. 2. Immunohistochemicalresults show that: Expresion of HSP70 positive cells was found after cerebral ischemia followdby reperfusion 6h in the penumbra zone,it reached a peak level at 24h after reperfusion(P<0.05),then declined.Expresion of HSP70 and TLR4 in NBP-pretreatment group at all time points weredistinctly lower than ischemia-reperfusion group(P<0.05).3. Ischemia-reperfusion group of thecontralateral cerebral hemisphere and sham operation group occasional apoptotic cells,speculatethat is physiological neuronal necrosis A large number of TUNEL-positive cells were observed inI-R group(P<0.05),TUNEL-positive cells were markly reduced in NBP treated group,but higherthan the sham group (P<0.05).Conclusion:1.Focal cerebral ischemia and reperfusion model were successfullyreplicated.the rats development typical symptoms of neurological impairment.HE staining resultsin line with pathological process.2.NBP-pretreatment could attenuate cell death aftercerebralischemia-referfusion,show a neuroprotictive effect.3.NBP-pretreatment obviouslyinhibited transient focal cerebral ischemia induced apoptosis in cortex and hippocampus, NBPpretreatmentobviously inhibited focial cerebral ischemia-reperfusion injury through downregulatethe expression of HSP70 and TLR4 ,and show a neuroprotective effect.