Neuroprotective effect of cerebral ischemic preconditioning is associated with regulation of expressions of nuclear factor-κB and Hes1 in rats / 国际脑血管病杂志

ABSTRACT

Objective To investigate the neuroprotective mechanism of cerebral ischemic preconditioning by detecting the expression changes of hippocampus nuclear factor-κB (NF-κB) and Hesl mRNA after cerebral ischemia-reperfusion in rats.Methods A total of 108 healthy male SD rats were randomly divided into a cerebral ischemia group,a cerebral ischemic preconditioning group,and a sham operation group,and then redivided into 22 h,48 h,72 h,7 d,and 14 d subgroups.Ischemic preconditioning was performed at day 3 before establishing the cerebral ischemia-reperfusion injury model by transient occlusion of right internal carotid artery for 10 min.At each time point after cerebral ischemia-reperfusion,the neurological deficit score and cerebral infarction volume measurement were performed,and the expressions of NF-κB and Hes1 mRNA in the hippocampus were detected by using real-time fluorescence quantitative polymerase chain reaction.Results The neurological function scores and the percentage of cerebral infarction volume in the cerebral ischemic preconditioning goup at each time point were significantly lower than those in the cerebral ischemia-reperfusion group (all P ＜0.05).The expression levels of NF-κB and Hesl mRNAs in each group had progressive reduction with time.Compared with the same time point,it showed that the expression levels of NF-κB and Hes1 mRNAs in the cerebral ischemic preconditioning group and the cerebral ischemia-reperfusion group were significantly higher than those in the sham operation group,the expression level of NF-κB mRNA in the cerebral ischemic preconditioning group was significantly lower than that in the cerebral ischemia-reperfusion group,and the expression level of Hesl mRNA was significantly higher than that in the cerebral ischemia-reperfusion group (all P ＜0.05).Conclusions The upregulation of Hesl and down-regulation of NF-κB may be involved in the neuroprotective mechanisms of cerebral ischemic preconditioning.