【摘 要】
：
目的 探讨脑蛋白水解液(CHI)对七氟醚麻醉导致的大鼠学习记忆障碍的影响,并分析其可能作用机制.方法 将32只大鼠随机分为七氟醚组、CHI高剂量组、CHI低剂量组和对照组,每组8
【机 构】
：
西安市交通大学医学院第一附属医院麻醉科,西安 710061;阿里地区人民医院手麻科,阿里 859000
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目的 探讨脑蛋白水解液(CHI)对七氟醚麻醉导致的大鼠学习记忆障碍的影响,并分析其可能作用机制.方法 将32只大鼠随机分为七氟醚组、CHI高剂量组、CHI低剂量组和对照组,每组8只.七氟醚组吸入2％ 七氟醚,每天2 h,连续7 d,CHI高剂量组每天吸入七氟醚之前,尾静脉注射脑蛋白水解液1200μL,CHI低剂量组每天吸入七氟醚之前,尾静脉注射脑蛋白水解液300μL.对照组不吸入七氟醚,尾静脉注射生理盐水.通过水迷宫实验记录大鼠学习记忆能力;HE染色法观察各组大鼠海马组织病理学改变;ELISA检测各组大鼠海马组织中MDA、SOD水平;TUNEL检测各组大鼠海马神经元细胞凋亡情况;RT-qPCR检测各组海马组织中SYT1 mRNA表达情况;Western blot检测各组大鼠海马组织中SYT1、Bax、Bcl-2、cleaved-Caspase3蛋白表达情况.结果 与对照组相比,七氟醚组大鼠逃避潜伏期显著增加(P<0.05),穿越平台次数显著减少(P<0.05),平台停留时间显著缩短(P<0.05),海马组织神经元细胞排列散乱,边界不清,细胞核固缩,出现空泡,着色较深,海马组织神经元细胞凋亡率显著升高(P<0.05),MDA、Bax、cleaved-Caspase3蛋白含量显著升高(P<0.05),SOD、Bcl-2、SYT1 mRNA和蛋白含量显著下降(P<0.05);与七氟醚组比,CHI高剂量组大鼠逃避潜伏期显著缩短(P<0.05),穿越平台次数显著增加(P<0.05),平台停留时间显著延长(P<0.05),海马组织神经元细胞排列相对紧密,胞核固缩和空泡现象得到改善,海马组织神经元细胞凋亡率显著下降(P<0.05),MDA、Bax、cleaved-Caspase3蛋白含量显著下降(P<0.05),SOD、Bcl-2、SYT1 mRNA和蛋白含量显著升高(P0.05).结论 七氟醚吸入前预先给予高剂量CHI能够改善七氟醚麻醉导致的大鼠学习记忆障碍,其机制可能与降低氧化应激损伤,抑制海马神经元细胞凋亡和增加SYT1表达有关.
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