microRNA-124通过调控PI3K/Akt2信号通路改善七氟醚诱导的新生大鼠神经缺陷  

microRNA-124 attenuates sevoflurane-induced neurological deficits in neonatal rats by regulating the PI3K/Akt2 signaling pathway

作　　者：李珍 张颖 屈青玲 LI Zhen;ZHANG Ying;QU Qing-ling(Anesthesiology Department,Qinghai Women's and Children's Hospital,Xining 810007;Liaoning Institute of Science and Technology,Benxi 117004,China)

机构地区：[1]青海省妇女儿童医院麻醉科,青海西宁810007 [2]辽宁科技学院,辽宁本溪117004

出　　处：《解剖科学进展》2022年第5期592-596,共5页Progress of Anatomical Sciences

基　　金：青海省自然科技攻关基金资助项目(201935011)。

摘　　要：目的探讨microRNA-124对七氟醚诱导新生大鼠神经缺陷的影响及可能机制。方法40只SD大鼠随机分为对照组(CON)、七氟醚组(SEV)、Agomir NC+SEV组、miR-124 Agomir+SEV组,每组10只。Morris水迷宫测试大鼠学习记忆能力;双染法检测海马神经元凋亡情况;RT-qPCR方法检测大鼠BDNF、PI3K、Akt2 mRNA的表达;Western blot检测海马组织中BDNF、PI3K、Akt2蛋白表达。结果与CON组比较,SEV组逃避潜伏期延长,目标象限时间百分比缩短,穿越平台次数减少,海马组织中BDNF、PI3K、Akt2蛋白表达降低(P<0.001),海马神经元细胞凋亡增加;与SEV组比较,miR-124 Agomir+SEV组目标象限时间百分比延长(P<0.01)、逃避潜伏期缩短(P<0.05),穿越平台次数增加(P<0.05),海马组织中BDNF、PI3K、Akt2蛋白表达升高(P<0.01),海马神经元细胞凋亡减少。结论miR-124可能通过调控PI3K/Akt2信号通路改善七氟醚诱导的大鼠神经功能缺陷。Objective To investigate the effect of microRNA-124 on sevoflurane induced neurologic defect in neonatal rats and its possible mechanism.Methods Forty SD rats were randomly divided into control group(CON),sevoflurane group(SEV),Agomir NC+SEV group and miR-124 Agomir+SEV group,with 10 rats in each group.The learning and memory ability of rats was observed by morris water maze.The apoptosis of hippocampal neurons was detected by double staining method.The expression of BDNF,PI3K and AKT2 mRNA was detected by RT-qPCR.The expression of BDNF,PI3K and AKT2 in hippocampus was detected by Western blot.Results Compared with the CON group,the escape latency of SEV group was prolonged,the target quadrant time percentage is reduced,the number of crossing platforms was decreased,expression of BDNF,PI3K and AKT2 protein in hippocampus was decreased(P<0.001),the apoptosis of hippocampal neurons was increased.Compared with the SEV group,the percentage of target quadrant time in the miR-124 Agomir+SEV group was longer(P<0.01),reduced escape latency(P<0.05),increased the number of crossing platforms(P<0.05),increased expression of BDNF,PI3K and AKT2 protein in hippocampus(P<0.01),decreased apoptosis of hippocampal neurons.Conclusion miR-124 may improve sevoflurane-induced neurological deficits in rats by regulating PI3K/Akt2 signaling pathway.

关 键 词：七氟醚 miR-124 PI3K/Akt2信号通路 神经元 

分 类 号：R614[医药卫生—麻醉学]