| 易菲妮,余贤君,马 超,陈秋霞,林慧娟,黄明伟.七氟醚通过调节JNK信号通路对幼鼠空间探索能力及认知功能的影响[J].,2020,(14):2629-2634 |
| 七氟醚通过调节JNK信号通路对幼鼠空间探索能力及认知功能的影响 |
| Effects of Sevoflurane on Spatial Exploration Ability and Cognitive Function in Young Rats by Regulating JNK Signaling Pathway |
| 投稿时间：2020-02-28 修订日期：2020-03-24 |
| DOI：10.13241/j.cnki.pmb.2020.14.006 |
| 中文关键词: 七氟醚 神经功能 海马体 凋亡 c-Jun氨基末端激酶 乙酰酰胆碱酯酶 胆碱乙酰转移酶 |
| 英文关键词: Sevoflurane Neural function Hippocampus Apoptosis c-Jun amino terminal kinase Acetylcholinesterase Choline acetyltransferase |
| 基金项目:福建省自然科学基金项目（2016J01575） |
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| 中文摘要: |
| 摘要 目的：探究七氟醚通过调节c-Jun氨基末端激酶（JNK）信号通路对幼鼠空间探索能力及认知功能的影响。方法：48只7 d日龄的SD大鼠随机分为3组：对照组、七氟醚组和七氟醚+SP600125组。七氟醚组和七氟醚+SP600125组吸入七氟醚，七氟醚+SP600125组使用JNK抑制剂SP600125灌胃。在最后一次吸入七氟醚3 h后每组随机处死8只幼鼠，通过TUNEL染色检测海马体神经元凋亡。在大鼠性成熟后通过水迷宫实验和跳台实验检测神经功能和学习能力。在吸入七氟醚后3 h和性成熟后通过Western blotting检测JNK和Caspase-3蛋白，并比较各组AchE和CHAT的活性。结果：在建模后3 h，七氟醚组的JNK、Caspase-3蛋白水平、AchE活性显著高于对照组，CHAT活性显著低于对照组（P<0.05）。七氟醚+ SP600125组的JNK、Caspase-3、AchE活性水平显著低于七氟醚组，CHAT活性显著高于七氟醚组（P<0.05）。七氟醚组幼鼠的海马体神经元凋亡率显著高于对照组（P<0.05），七氟醚+SP600125组的凋亡率显著低于七氟醚组（P<0.05）。在大鼠性成熟后与对照组比较，七氟醚组的逃避潜伏期升高而穿越平台次数降低，错误次数显著升高而潜伏期显著降低（P<0.05），并且七氟醚+SP600125组的逃避潜伏期低于七氟醚组而穿越平台次数高于七氟醚组，错误次数显著低于七氟醚组而潜伏期显著高于七氟醚组（P<0.05）。各组大鼠性成熟后海马体中JNK和Caspase-3蛋白水平比较差异无统计学差异（P>0.05）。性成熟后各组大鼠海马体中AchE活性比较差异不显著（P>0.05）。七氟醚组的CHAT水平显著低于对照组（P<0.05），七氟醚+ SP600125组的CHAT水平显著高于七氟醚组（P<0.05）。结论：七氟醚可能通过激活JNK通路促进海马体神经元细胞凋亡，并使AChE活性升高而ChAT活力降低，导致大鼠神经功能、学习和记忆力降低。 |
| 英文摘要: |
| ABSTRACT Objective: To investigate the effects of sevoflurane on the spatial exploration ability and cognitive function of young rats by regulating the c-Jun amino terminal kinase (JNK) signaling pathway. Methods: Forty-eight 7-day-old SD rats were randomly divided into three groups: the control group, the sevoflurane group, and the sevoflurane + SP600125 group. The sevoflurane group and the sevoflurane + SP600125 group inhaled sevoflurane. In the sevoflurane + SP600125 group, the JNK inhibitor SP600125 was administered to the stomach. Eight young rats in each group were sacrificed at random 3 h after the last inhalation of sevoflurane. Apoptosis of hippocampal neurons was detected by TUNEL staining. After sexual maturity in rats, neural function and learning ability were measured by water maze experiments and platform jumping experiments. Western blotting was used to detect JNK and Caspase-3 protein 3 h after sevoflurane inhalation and sexual maturity, and the activities of AchE and CHAT in each group were compared. Results: Three hours after modeling, JNK, Caspase-3 protein levels, and AchE activity were significantly higher in the sevoflurane group than in the control group, and CHAT activity was significantly lower than the control group (P<0.05). The levels of JNK, Caspase-3, and AchE in the sevoflurane + SP600125 group were significantly lower than those in the sevoflurane group, and the CHAT activities were significantly higher than those in the sevoflurane group (P<0.05). The apoptosis rate of hippocampal neurons in the sevoflurane group was significantly higher than that in the control group (P<0.05). The apoptosis rate of the sevoflurane + SP600125 group was significantly lower than that of the sevoflurane group (P<0.05). After sexual maturity in rats, compared with the control group, the escape latency of the sevoflurane group increased and the number of crossing platforms decreased, the number of errors increased significantly, and the latency decreased significantly (P<0.05). The escape latency of the sevoflurane + SP600125 group was lower than that of the sevoflurane group and the number of crossing platforms was higher than that of the sevoflurane group. The number of errors was significantly lower than that of the sevoflurane group and the latency was significantly higher than that of the sevoflurane group (P<0.05). There was no significant difference in the levels of JNK and Caspase-3 protein in the hippocampus of each group after sexual maturity (P>0.05). There was no significant difference in AchE activity between hippocampus of each group after sexual maturity (P>0.05). The level of CHAT in the sevoflurane group was significantly lower than that in the control group (P<0.05). The level of CHAT in the sevoflurane + SP600125 group was significantly higher than that in the sevoflurane group (P<0.05). Conclusion: Sevoflurane may promote hippocampal neuronal apoptosis through activation of the JNK pathway, increase AChE activity and decrease ChAT activity, leading to reduced neurological function, learning and memory in rats. |
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