Arachidonic acid attenuates learning and memory dysfunction induced by repeated isoflurane anesthesia in rats

被引:1
作者
Li, Chunjiang [1 ]
Wang, Qingwei [2 ]
Li, Lanlan [3 ]
Liu, Yun [4 ]
Diao, Hongwei [1 ]
机构
[1] Heilongjiang Prov Hosp, Nangang Branch, Dept Anesthesiol, Haerbin 150001, Heilongjiang, Peoples R China
[2] Haerbin First Hosp, Dept Anesthesiol, Haerbin 150010, Peoples R China
[3] Heilongjiang Prov Hosp, Dept Anesthesiol, Haerbin 150001, Heilongjiang, Peoples R China
[4] Heilongjiang Eye Dis Prevent Inst, Dept Ophthalmol, Haerbin 150001, Peoples R China
来源
INTERNATIONAL JOURNAL OF CLINICAL AND EXPERIMENTAL MEDICINE | 2015年 / 8卷 / 08期
关键词
ARA; isoflurane anesthesia; learning and memory dysfunction; cholinergic system; Glu/GABA regulatory system; COGNITIVE DYSFUNCTION; ALZHEIMERS-DISEASE; CASPASE ACTIVATION; OXIDATIVE STRESS; IMPAIRMENT; SUPPLEMENTATION; HIPPOCAMPUS; APOPTOSIS; FAMILY;
D O I
暂无
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
This study aims to explore the effects of arachidonic acid (ARA) on learning and memory dysfunction in rats exposed to repeated isoflurane anesthesia and the underlying mechanisms. Fifty rats were randomly divided into five groups: sham control group, isoflurane group, low dose ARA + isoflurane group, moderate dose ARA + isoflurane group, high dose ARA + isoflurane group. The Morris water maze test was performed to assess learning and memory function and the hippocampus tissues were obtained for biochemical analysis. The results showed that administration of ARA improved learning and memory deficit induced by repeated isofluane anesthesia in Morris water maze test and in a dose-dependent manner. Additionally, ARA increased the activities of choline acetyl transferase (ChAT), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and the levels of acetycholine (Ach) and.-amino-butyric acid (GABA), whereas decreased the activity of acetylcholine esterase (AchE), the content of glutamate (Glu) and malondialdehyde (MDA), and the radio of Glu/GABA. Meanwhile, ARA elevated the ratio of Bcl-2/Bax and inhibited the activity of caspase-3. In conclusion, ARA has potential therapeutic value in alleviating isoflurane-induced learning and memory impairment. The mechanism might be involved in regulating the cholinergic and Glu/GABA regulatory system, decreasing oxidative damage and inhibiting cell apoptosis.
引用
收藏
页码:12365 / 12373
页数:9
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