Expression And Signiificance Of Nudear Factor-kappaBp65 And Intercellular Adhesion Molecule-1 Following Ischemic Preconditioning

Objective: 1. To investigate the protection and the positive significance of the ischemic preconditioning on the pMCAO. 2 To investigate the ischemic Tolerance and the developing expression of NF-kB,ICAM-1, the correlation betwine them after ischemic preconditioning. 3 The investigate the expression and significance of NF-kB ICAM -1 following the ischemic Tolerance indued by ischemic preconditioning.Methods: 1. To establish the cerebral ischemia precondition model and the pMCAO model. 2. Wistar rats were randomly divided into four groups: normal group (group S ), preconditioning group (group IP), pMCAO group (group R ), pMCAO after preconditioning group, (group IPR ) to observe Neurological deficits according to the Longa s score. cerebral infarction volume ratio and cerebral tissue damaging status at the corresponding timepoin .3. Pathematologymorph was observe d by HE staining,The expression of NF-JcB and ICAM-1 was detected by immunohistochemistry,Results: 1. Ischemic preconditioning can induce ischemic Tolerance, the Neurological deficits score is decreesed significantly.( P<0. 05) at the same timepoint. 2 The non- ischemic area in group S,IP,R was dyed schillerization by TTC, the Infarct district was white color, ischemic preconditioning reduce brain injured, cerebral infarction volume ratio in group IPR was less significantly than that in group R (P<0. 05)3. The immunohistochemical results showed that the expressions of NF—KB was low in the group S and group IP, while which increased from 6 h after ischemic in the group R and group IPR, it reached the summit at 24h when it was delayde at 48h in group IPR and then fell off gradually (P<0. 05), the group IPR was less significantly than the group R at any time ( P<0. 05).4 The expressions of ICAM -1 inthe group S and group IP in the ischemic cortical area and basal ganglia were little( P>0. 05), when in the group R and group IPR the expressions increased from 6 h after ischemic and reached the summit at 48h (?<0. 05), and then fell off gradually in group R, but stayed high level in the the group IPR at 48-72h ;at the same timepoint 6h-48h, the group IPR was less significantly than the group R (P<0. 05), when not at 72h (P>0.05 ) .Conclusion: 1 .In the animal experiment, ischemic precondition can prime endogenous protection, decrease brain injured, it can induce ischemic Tolerance. 2 Ischemic precondition can lessen neurologic impairment, reduce Infarct volume, decrease the expressions of NF—KB and ICAM-1, delay the apex time of expression, enhance the cerebral ischemia Tolerance competence . 3 The expressions of NF-κB and ICAM-1 were significant deviation interclass at the same timepoint, which indicamed that inhibition Inflammatory reaction may be one of the mportant molecule mechanism of the ischemic Tolerance induced by ischemic precondition...