Effect of sevoflurane post-conditioning on PARP expression in cerebral cortex during focal cerebral ischemia/reperfusion in rats / 中华麻醉学杂志

ABSTRACT

Objective To investigate the effect of sevoflurane post-conditioning on the expression of poly (ADP-ribose) polymerase (PARP) in the cerebral cortex during focal cerebral ischemia/reperfusion (I/R) in rats and the mechanism.Methods Fifty-four male Sprague-Dawley rats,weighing 250-320 g,were randomly divided into3 groups (n =18 each) using a random number tablesham operation group (S group),I/R group and sevoflurane post-conditioning group (Sevo-pc group).The animals were anesthetized with intraperitoneal chloralhydrate 300 mg/kg.In Sevo-pc and I/R groups,focal cerebral ischemia was induced by middle cerebral artery occlusion using a nylon thread with rounded tip inserted into the right internal carotid artery and advanced cranially until resistance was met.The occlusion was maintained 1 h,followed by 24 h reperfusion.The animals in Sevo-pc group inhaled 2.7％ sevoflurane for 1 h starting from onset of reperfusion.At 24 h of reperfusion,neurological deficits were assessed,and then the rats were decapitated.The brains were immediately harvested for determination of the cerebral infarct size (by TTC staining) and expression of PARP in the ischemic cerebral cortex (by immunohistochemistry).The number of apoptotic cells was counted using TUNEL.The apoptosis index was calculated.Results Compared with group S,the neurological deficit scores and apoptotic cells were significantly increased,the cerebral infarct size was enlarged,and the expression of PARP in the ischemic cerebral cortex was up-regulated in I/R and Sevo-pc groups (P ＜ 0.05 or 0.01).The neurological deficit scores and apoptotic cells were significantly lower,the cerebral infarct size was smaller,and the expression of PARP in the ischemic cerebral cortex was downregulated in Sevo-pc group (P ＜ O.05 or 0.01).Conclusion Sevoflurane post-conditioning can reduce focal cerebral I/R injury in rats and down-regulation of PARP expression in the cerebral cortex may be involved in the mechanism.