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目的:观察异氟烷对幼鼠学习记忆能力的影响及海马组织凋亡的影响。方法:2019年5月到2020年6月购自河南实验动物中心的60只幼年SD大鼠随机分对照组、异氟烷1 h组和异氟烷3 h组。对照组不做处理，异氟烷1 h组和异氟烷3 h组分别在35 ℃恒温下采用1.5%异氟烷麻醉1 h和3 h，并自主苏醒。采用Morris水迷宫实验检测幼鼠空间学习记忆能力；采用原位缺口末端标记法(TUNEL)染色分析3组大鼠海马组织细胞凋亡水平；采用酶联免疫法测定每组大鼠血清氧化应激指标变化；采用蛋白质印迹法(Western blot)分析海马组织生存素(Survivin)和半胱氨酰天冬氨酸特异性蛋白酶(Caspase)-3蛋白表达水平。组间比较采用单因素方差分析，组间两两比较采用LSD法。结果:与对照组逃避潜伏期和穿台指数[(6.89±2.14) s、(6.24±1.65)次]比较，异氟烷1 h组和异氟烷3 h组幼鼠逃避潜伏期[(10.25±2.78)、(14.95±3.82) s]明显增加，而穿台指数[(4.29±1.20)、(3.01±0.89)次]明显下降，差异均有统计学意义(n t＝4.025，n P<0.05；n t＝3.718，n P<0.05；n t＝2.594，n P<0.05；n t＝2.514，n P<0.05)。与对照组[(7.41±0.61) nmol/ml和(102.39±7.98) U/ml]比较，异氟烷1 h组幼鼠MDA水平[(10.49±1.42) nmol/ml]显著增加，超氧化物歧化酶(SOD)水平[(79.42±5.81) U/ml]显著下调，差异均有统计学意义(n t＝3.110、2.901，n P<0.05)。与异氟烷1 h组比较，异氟烷3 h组幼鼠MDA水平[(14.81±1.97) nmol/ml]显著增加，SOD水平[(50.22±4.89) U/ml]显著下调，差异均有统计学意义(n t＝2.619、2.211，n P<0.05)。与对照组[(3.28±0.89)%]比较，异氟烷1 h组幼鼠海马组织细胞凋亡比例[(12.56±3.21)%]显著增加，差异均有统计学意义(n t＝3.103，n P<0.05)。与异氟烷1 h组比较，异氟烷3 h组海马组织细胞凋亡比例[(14.81±1.97)%]显著增加，差异均有统计学意义(n t＝2.901，n P<0.05)。与对照组[(0.30±0.11)、(0.94±0.11)]比较，异氟烷1 h组幼鼠海马组织Caspase-3表达水平[(0.93±0.14)]显著增加，而Survivin蛋白表达水平[(0.60±0.10)]显著下调，差异均有统计学意义(n t＝3.481，n P<0.05；n t＝2.954，n P<0.05)。与异氟烷1 h组比较，异氟烷3 h组幼鼠海马组织Caspase-3表达水平[(1.61±0.21)]显著增加，而Survivin蛋白表达水平[(0.18±0.08)]显著下调，差异均有统计学意义(n t＝2.471，n P<0.05；n t＝2.169，n P<0.05)。n 结论:异氟烷可诱导幼鼠机体氧化应激，促进脑细胞凋亡，进而影响学习和记忆能力。“,”Objective:To investigate the effects of isoflurane on learning and memory ability and hippocampal apoptosis in young rats.Methods:60 young SD rats from May 2019 to June 2020 were randomly divided into control group, isoflurane 1 h group and isoflurane 3 h group. Rats in the control group was not treated. Rats in isoflurane 1 h group and isoflurane 3 h group were anesthetized with 1.5 % isoflurane at 35 ℃ for 1 h and 3 h, respectively, and then they recovered spontaneously. The spatial learning and memory ability of young rats were analyzed by Morris water maze test. The apoptosis level of nerve cells in the three groups were analyzed by terminal-deoxynucleotidyl transferase mediated nick end labeling (TUNEL) staining. The changes of serum oxidative stress indexes were analyzed by enzyme linked immunosorbent assay (ELISA). The expression levels of survivin and cysteinyl aspartate-specific protease (Caspase)-3 in hippocampus were analyzed Western blotting.Results:Compared with the control group, the escape latency period [(10.25±2.78), (14.95±3.82) s] significantly increased, while wear index [(4.29±1.20), (3.01±0.89) times] significantly decreased in isoflurane 1 h group and in isoflurane 3 h group(n t=4.025, 3.718, 2.594, 2.514, n P<0.05). Compared with the control group [(7.41±0.61) nmol/ml and (102.39±7.98) U/ml], the level of MDA [(10.49±1.42) nmol/ml] in isoflurane 1 h group was significantly higher [(79.42±5.81) U/ml] (n t=3.110, n P<0.05;n t=2.901, n P<0.05). Compared with 1 h isoflurane group, the level of MDA [(14.81±1.97) nmol/ml] in isoflurane 3 h group was significantly increased, and SOD level [(50.22±4.89) U/ml] was significantly decreased (n t=2.619, n P<0.05;n t=2.211, n P<0.05). Compared with the control group [(3.28±0.89)%], the apoptosis rate of hippocampal tissue [(12.56±3.21)%] in isoflurane 1 h group was significantly increased (n t=3.103, n P<0.05). Compared with isoflurane 1 h group, the apoptosis rate of hippocampal tissue in isoflurane 3 h group [(14.81±1.97)%] significantly increased (n t=2.901, n P<0.05). Compared with the control group [(0.30±0.11), (0.94±0.11)], the expression of Caspase-3 [(0.93±0.14)] significantly increased in isoflurane 1 h group, while the expression of survivin protein [(0.60±0.10)] significantly decreased (n t=3.481, n P<0.05;n t=2.954, n P<0.05). Compared with isoflurane 1 h group, Caspase-3 expression level [(1.61±0.21)] in isoflurane 3-hour group was significantly increased, while survivin protein expression level [(0.18±0.08)] was significantly decreased (n t=2.471, n P<0.05;n t=2.169, n P<0.05).n Conclusion:Isoflurane can induce oxidative stress, promote brain cell apoptosis, and then affect learning and memory ability.