| Objective: To study the role of p38MAPK signal pathway in the protectivemechanism of limb postconditioning against rat cerebral ischemia-reperfusioninjury.Methods: In this experiment, rats were randomly divided into4groups,which were sham operated group(sham group), ischemia reperfusion group (I/Rgroup), limb ischemic post-conditioning group(LPostC group) and limbischemic post-conditioning group+SB203580(LPostC+SB group). The focalmiddle cerebral artery occlusion(MCAO) model was made by suture-occludedmethod. After2h MCAO following24h of reperfusion, the neurological deficitscores were evaluated, the pathological changes of cerebral cortex wereobserved with HE staining. We investigated the expression of p-ATF-2withusing immunohistochemistry and p-p38MAPK expression in the frontal andparietal cortex with using western blot. Neuronal apoptosis was investigatedwith TUNEL. Results:(1) Compared with that of sham group, neurologlcaldeficits scores and cerebral ischemic injury of I/R group increased significantly;Compared with that of I/R group, neurologlcal deficits scores and cerebralischemic injury of LPostC group and LPostC+SB group reduced (all P<0.05).(2)Compared with that of sham group, neuronal apoptosis of I/R group increasedsignificantly; Compared with that of I/R group, neuronal apoptosis of LPostCgroup and LPostC+SB group reduced; Compared with that of LPostC group,neuronal apoptosis of LPostC+SB group reduced.(3) Compared with that of sham group, the expression of p-p38MAPK and p-ATF-2of I/R group increasedsignificantly; Compared with that of I/R group, the expression of p-p38MAPKand p-ATF-2of LPostC group and LPostC+SB group reduced; Compared withthat of LPostC group, the expression of p-p38MAPK and p-ATF-2ofLPostC+SB group reduced (all P<0.05). Conclusions: LPostC may obviouslyreduce cerebral ischemia-reperfusion injure by inhibiting the induction ofp-ATF-2expression and cell apoptosis through the blocking of the p38MAPKactivation. |
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