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作 者:吴建楠 周琪[1] 梁晓东[1] 宋健楠[1] 李海波[1] 张析哲[1] WU Jiannan;ZHOU Qi;LIANG Xiaodong;SONG Jiannan;LI Haibo;ZHANG Xizhe(Department of Anesthesiology,Municipal Hospital of Chifeng,Chifeng 024000 China)
出 处:《内蒙古医学杂志》2023年第5期528-531,共4页Inner Mongolia Medical Journal
摘 要:目的探讨右美托咪定预处理对老年术后认知功能障碍(POCD)大鼠工作记忆损伤的影响。方法选择健康雄性SD大鼠18只,18月龄,体质量500~550 g,采用随机数表法分为3组(n=6):对照组(C组)、手术组(S组)和右美托咪定预处理组(DP组)。各组实验鼠用Morris水迷宫进行5 d工作记忆训练后,S组和DP组行脾切除制作POCD模型。DP组于术前30 min腹腔注射右美托咪定12μg/kg,术后第7日进行工作记忆测试。以心尖取血法采集血样,ELISA法检测血浆IL-1β、IL-6和TNF-α浓度,采用Western blot检测海马区BDNF蛋白含量。结果在训练期,实验鼠第二组逃避潜伏期较第一组缩短;在测试期,与C组相比较,S组和DP组逃避潜伏期延长,达标前测试次数增加,海马区BDNF含量降低,血浆IL-1β、IL-6和TNF-α浓度增加;与S组比较,DP组逃避潜伏期缩短,达标前测试次数减少,海马区BDNF含量增加,血浆IL-1β、IL-6和TNF-α浓度降低(P<0.05)。结论右美托咪定可通过降低炎症反应、增加海马区BDNF表达而改善老年POCD大鼠工作记忆损伤。Objective To evaluate the effect of dexmedetomidine pretreatment on working memory deficit in aged mice with postoperative cognitive dysfunction.Methods Eighteen healthy male Sprague-Dawley rats,aged 18 months,weighing 500-550g,were divided into 3 groups(n=6 each)using a random table method:control group(C group),surgery group(S group)and dexmedetomidine pretreatment group(DP group).After 5 days of working memory training with Morris water maze in each group,POCD models were established by splenectomy.Dexmetomidine 12μg/kg was intraperitoneally injected at 30 min before removed spleen.Working memory test at 7 day after operation.The animals were sacrificed after the end of working memory test,blood samples were collected from hearts,IL-1β、IL-6 and TNF-αconcentration were detected by ELISA,brains were removed and hippocampl were isolated for determination expression of BDNF.Results During training days,the escape latency were significantly reduced in the second block compared with the first block,During the working memory test days,compared with group C,the escape latency was significantly prolonged after operation,required significantly more trials to reach criterion,the expression of BDNF was down-regulated,IL-1β.IL-6 and TNF-αconcentration was increased in the group S and DP.compared with group S,the escape latency was significantly shortened after operation,required significantly lower trials to reach criterion,the expression of BDNF was up-regulated,IL-1β、IL-6 and TNF-αconcentration was decreased in the group DP(P<0.05).Conclusion The mechanism by which dexmedetomidine pretreatment mitigates working memory deficit be related to reducing inflammatory response and up-regulating the expression of BDNF in hippocampl of elderly POCD rats.
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