中国病理生理杂志2023，Vol.39Issue(4)：599-607,9.DOI:10.3969/j.issn.1000-4718.2023.04.003
自由基在肢体缺血预处理诱导的大鼠脑缺血耐受中的作用
Role of free radicals in cerebral ischemic tolerance of rats induced by limb ischemic preconditioning
摘要
Abstract
AIM: To explore whether free radicals participate in cerebral ischemic tolerance and the up-regula-tion of p38 MAPK and ERK signaling pathways in rats induced by limb ischemic preconditioning (LIP). METHODS: A total of 128 Wistar rats with permanent occlusion of bilateral vertebral arteries were randomly divided into sham group (n=16), cerebral ischemia (CI) group (n=16), LIP+CI group (n=16), DMTU (a free radical scavenger)+LIP+CI group (n=64) and DMTU+sham group (n=16). Six rats in each group were used to observe the delayed neuronal death (DND) in hippocampal CA1 region by thionin staining at 7 d after the end of operation. Other 10 rats in each group were used to de-tect the expression of p38 MAPK and ERK in hippocampal CA1 region by immunohistochemistry and Western blot. RE-SULTS: Lethal CI resulted in obvious DND in hippocampal CA1 region. However, LIP reversed the above injurious changes, represented by the decrease in histological grade and the increase in neuronal density compared with CI group (P<0. 01). Moreover, LIP significantly up-regulated the expression of p38 MAPK and ERK in hippocampal CA1 region com-pared with CI group (P<0. 01). Administration of free radical scavenger DMTU via femoral vein before LIP partially re-versed the neuroprotective effect of LIP, and blocked the up-regulation of p38 MAPK and ERK expression in hippocampal CA1 region in rats compared with LIP+CI group (P<0. 01). CONCLUSION: Free radicals are involved in the neuropro-tection and up-regulation of p38 MAPK and ERK expression induced by LIP in rats.关键词
自由基/肢体缺血预处理/脑缺血耐受/p38 MAPK信号通路/ERK信号通路Key words
free radicals/limb ischemic preconditioning/cerebral ischemic tolerance/p38 MAPK signaling pathway/ERK signaling pathway分类
医药卫生引用本文复制引用
冯荣芳,袁强,张晓,李淑琴,孙晓彩..自由基在肢体缺血预处理诱导的大鼠脑缺血耐受中的作用[J].中国病理生理杂志,2023,39(4):599-607,9.基金项目
Supported by grants from National Natural Science Foundation of China(No.31100781)and Natural Science Foundation of Hebei Province,China(No.C2011206040). （No.31100781）
