Expression Of TLR4、NF-κB And Trif In Rat With Focal Cerebral Infarction After Ischemic Preconditioning

Objectives：Ischemic tolerance in the brain, in which brief ischemia increasesresistance to subsequent injurious ischemia is a powerful adaptive defence thatinvolves an endogenous programme of neuroprotection. However, the precisemechanisms that underlie these neuroprotective processes are not completelydefined. The present experiment was conducted to investegate the expression ofTLR4、NF-κB and TRIF in rat model of ischemic preconditioning, to explore thepossible mechanisms of neuroprotection on brain ischemic tolerance.Methods：90healthy male adult Sprague-Dawley rats were divided into threeexperimental groups randomly, the ischemic preconditioning and middlecerebral artery occlusion (MCAO) group (IP+MCAO, n=40), the sham andMCAO group (SS+MCAO, n=40) and the sham surgery group (SS+SS, n=10).The first two groups were further divided into four subgroups respectively fordifferent preconditioning ischemia intervals. Models of cerebral ischemicpreconditiong and ischemic reperfusion were made by twice suture method.Transient MCAO(10mins) was used for IP and48h reperfusion was allowedafter IP and before MCAO to establish IT. The neurological deficits, brain watercontent, the infarct volume and the histological findings with HE staining wereexamined. The expression of TLR4、 NF-κB and TRIF were determined bymethods of immunohistochemistry and reverse transcriptase polymerase chainreaction respectively. Results：The rats of neurological deficits, brain water content and the infarct volumein experimental group were reduced significantly compared with control group.Meanwhile the brain edema was alleviated and the histological injury were mildin experimental group. There were significant differences between experimentalgroup and control group(P<0.05). The protein expression of TLR4、NF-κB andTRIF in groups of IP+MCAO and SS+MCAO were higher compared with shamoperated group, moreover, the TRIF was higher in experimental group andTLR4、 NF-κB were higher in control group. There were significant differencesamong two groups (P<0.05).Conclusion：Ischemic preconditioning induced ischemic tolerance and providedprotective effects on brain in rat. It suggested that TLR4was an essentialmediator on cerebral ischemic tolerance and the mechanism might correlatedwith the higher expression of TRIF and the lower expression of NF-κB.