目的 探讨七氟醚通过上调MicroRNA-96(miR-96)影响大鼠认知障碍的效果与机制.方法 健康清洁级雄性SD大鼠15只随机数字表法分为3组,每组5只,分别为对照组、七氟醚暴露4 h组(实验1组)、七氟醚暴露8h组(实验2组),对照组在相同的环境下吸入2 L/min氧气8 h,实验1组停止吸入七氟醚后吸入2 L/min氧气4 h.采用水迷宫实验测定大鼠认知功能,检测不同时间点的认知功能、血气指标、体温、血清IGF-1水平和miR-96表达情况.结果 实验1组与实验2组麻醉后3 d、7 d与14 d的逃避潜伏期显著高于对照组,目标象限累计时间低于对照组,比较差异有统计学意义(P ＜0.05),实验1组与实验2组比较差异也有统计学意义(P ＜0.05).三组大鼠PaO2与体温在麻醉前、麻醉4 h与麻醉8 h的组内与组间比较差异无统计学意义(P＞ 0.05).实验1组与实验2组麻醉后3 d、7d与14 d的血清IGF-1含量均显著低于对照组(P ＜0.05),实验2组显著低于实验1组(P ＜0.05).实验1组与实验2组麻醉后7 d海马组织的miR-96相对表达量显著低于对照组(P ＜0.05),实验2组显著低于实验1组(P ＜0.05).结论 七氟醚能通过上调大鼠海马组织miR-96的表达,抑制血清IGF-1的表达,从而损伤大鼠的认知功能,且七氟醚暴露8 h较暴露4 h对其损伤更明显.%Objective To investigate the effect and mechanism of sevoflurane on up-regulating microRNA-96 (miR-96) in regulating cognitive impairment in rats. Methods 15 healthy and clean male SD rats were randomly divided into 3 groups, 5 rats in each groups, including the control group, sevoflurane exposed for 4 h (experiment group 1) and sevoflurane exposed for 8 h (experiment group 2), the control group were inhaled 2 L/min oxygen for 8 hours under the same environment, and the experimental group 1 stopped inhaling sevoflurane and inhaled 2 L/min oxygen for 4 hours. The water maze test were used to determine the cognitive function of the rats, and the miR-96 expression were detected. Results The escape latency of the experimental group 1 and the experimental group 2 were significantly higher than that of the control group at 3 d, 7 d and14 d after anesthesia. The cumulative time of the target quadrant were lower than that of the control group with statistically significant difference (P＜ 0. 05)). There were no significant difference in PaO2 and body temperature compared among the three groups before the anesthesia, 4 h anesthesia and 8 h anesthesia (P＞ 0. 05). The levels of serum IGF-1 in the experimental group 1 and the experimental group 2 were significantly lower than those in the control group at 3 d, 7 d and 14 d after anesthesia (P ＜ 0. 05). The experimental group 2 were significantly lower than the experimental group 1 (P ＜ 0. 05). The relative expression of miR-96 in hippocampus at 14 d after anesthesia of experimental group 1 and experimental group 2 were significantly lower than that of the control group (P ＜ 0. 05). The experimental group 2 were significantly lower than the experimental group 1 (P ＜0. 05). Conclusion Sevoflurane can up-regulate the expression of miR-96 in rat hippocampus and inhibit the expression of serum IGF-1, thus impairing the cognitive function of rats. And the sevoflurane exposure for 8 h is more obvious than the exposure for 4 h.
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