Effect Of Ischemic Preconditioning On Cytochrome C And AIF Expression In Rats Subjectes To Cerebral Ischermic And Reperfusion

Objective To explore the brain protection effect of ischemic precondition by observingits effect on rat neurological function deficit score, cerebral infarction volume,pathological lesions and expression changes of cytochrome C (CytC) and apoptosisinducing factor (AIF) at the cortex region around infarction area and hippocampal CA1region after focal cerebral ischemia reperfusion.Methods Suture method was adopted to establish modified focal cerebral ischemiareperfusion model using male SD rats.100rats were randomly divided into shamoperation group (group SO), ischemic group (group MCAO) and ischemicpreconditioning group (group BIP). Rats in MCAO and BIP groups were under ischemiafor2h before reperfusion and then5rats at2h,6h,12h,24h,48h and72h were killedrespectively. Then for each of the above2groups,5more rats were killed at6h,24h and72h after reperfusion, respectively, for TTC staining so as to determine the volume ofcerebral infarction.5rats in SO group were killed at24h for TTC staining. Neurologicalfunction deficit score, brain tissue HE staining for pathological changes, TUNEL stainingfor observation of apoptotic neuron numbers in cortical and hippocampal CA1regionaround ischemic foci and expression of CytC and AIF in positive neurons at cortical andhippocampal CA1region around ischemic foci were undertaken and determined.Results1neurological function deficit score, cerebral infarction volume and braintissue pathomorphological observation: neurological function deficit, cerebral infarctionfoci and brain tissue pathomorphological changes were not observed in SO group.Compared with MCAO group, rats of BIP group had lower neurological function deficitscore, lower ischemic foci volume ratio and milder brain tissue pathological changes.21~2TUNEL staining positive neurons at cortical and hippocampal CA1regions wereobserved in SO group. The numbers of TUNEL staining positive neurons at cortical andhippocampal CA1regions started to increase at2h after ischemic reperfusion in MCAOand BIP groups and the numbers increased following time till at24h when it reached apeak and then decreased while adjacent time points comparison showed significantdifference(p<0.05). The numbers of TUNEL staining positive neurons at cortical andhippocampal CA1regions around ischemic foci at the same time points were lower inBIP group than that of MCAO group which showed significant difference(p<0.05).Compared with SO group, the numbers of TUNEL staining positive neurons at each timepoints in MCAO and BIP groups showed higher expression level which showedsignificant differences(p<0.05).3Small amount of CytC positive neurons were observedat cortical and hippocampal CA1regions in SO groups; the numbers of CytC positive neurons in MCAO and BIP groups started to increase at2h after ischemic reperfusion andshowed a rising trend as time went on. The numbers reached a peak at24h and thenumbers at adjacent time points showed significant differences (p<0.05); CytC positiveneurons at cortical and hippocampal CA1regions around ischemic foci in BIP group atthe same time point were lower than that of MCAO group which showed significantdifference(p<0.05); compared with SO group, CytC positive neurons at each time pointsin MCAO and BIP groups showed higher expression level which showed significantdifferences(p<0.05).4Small amount of AIF positive neurons were observed at corticaland hippocampal regions in SO group; AIF positive neurons in MCAO and BIP groupsshowed similar trend, which increased at2h after ischemic reperfusion and exhibited arising trend as time went on. The expression level reached a peak at48h at cortical regionand at24h at hippocampal CA1region and adjacent points comparison showedsignificant difference (p<0.05). the AIF positive neuron numbers at cortical andhippocampal CA1region around ischemic foci in BIP group at the same time wasevidently lower when compared with that of MCAO group and showed significantdifference (p<0.05); compared with SO group, AIF positive neurons at each time pointsin MCAO and BIP groups showed higher expression level which showed significantdifference (p<0.05).Conclusion1Focal cerebral ischemic reperfusion after ischemic preconditioningexhibited lower neurological function deficit score, reduced cerebral infarction volumeand milder brain tissue histopathological changes, which effectively reduced cerebralischemic reperfusion injury.2neuron apoptosis was reduced at cortical and hippocampalCA1regions around ischemic foci in cerebral ischemic reperfusion rat after ischemicpreconditioning, which protected brain from injury.3The expression of CytC and AIFwere reduced at cortical and hippocampal CA1regions around ischemic foci in cerebralischemic reperfusion rat after ischemic preconditioning and apoptosis might be inhibitedby inhibiting the expression of CytC and AIF.Figure92, Table8, Reference87.