Alpha 7 nicotinic acetylcholine receptor agonist GTS-21 mitigates isoflurane-induced cognitive impairment in aged rats

被引:35
|
作者
Kong, Fei-Juan [1 ,2 ]
Ma, Lei-Lei [3 ]
Zhang, Hong-Hai [2 ]
Zhou, Jia-Qiang [1 ]
机构
[1] Zhejiang Univ, Sch Med, Sir Run Run Shaw Hosp, Dept Endocrinol, Hangzhou 310016, Zhejiang, Peoples R China
[2] Nanjing Med Univ, Hangzhou Peoples Hosp 1, Dept Anesthesiol, Hangzhou, Zhejiang, Peoples R China
[3] Fudan Univ, Zhongshan Hosp, Shanghai Inst Cardiovasc Dis, Dept Cardiol, Shanghai, Peoples R China
基金
中国国家自然科学基金;
关键词
Alpha 7 nicotinic acetylcholine receptor; Isoflurane; Learning and memory; Apoptosis; Aged rats; NEUROCOGNITIVE FUNCTION; ALZHEIMERS-DISEASE; LEARNING-DEFICITS; POSTNATAL MEMORY; DYSFUNCTION; ANESTHESIA; EXPOSURE; SURGERY; MICE; NEUROINFLAMMATION;
D O I
10.1016/j.jss.2014.09.043
中图分类号
R61 [外科手术学];
学科分类号
摘要
Background: Postoperative cognitive dysfunction is increasingly recognized as an important clinical syndrome. Inhalation anesthetics are commonly used during surgery, and it has been proposed that inhalation anesthetics impair cognitive function. However, there are few clinical interventions and treatments available to prevent this disorder. GTS-21, a selective agonist of alpha 7 nicotinic acetylcholine receptor, has been indicated to exert neuroprotective effects in the experimental animal models of neurodegenerative diseases. Therefore, we hypothesized that pretreatment with GTS-21 attenuates isoflurane-induced cognitive decline in aged rats. Methods: In the present study, 20-mo-old rats were administered GTS-21or an equal volume of saline by intraperitoneal injection 30 min before exposure to isoflurane. Then the rats were exposed to 1.3% isoflurane for 4 h. Spatial learning and memory of the rats were assessed at 2 wk after isoflurane exposure. The expression levels of interleukin (IL)-1 beta, IL-6, and tumor necrosis factor-a in the hippocampus and cerebral cortex were determined by enzyme-linked immunosorbent assay. Simultaneously, neuronal apoptosis in the hippocampus was also observed by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) staining and Nissl staining. Results: We found that exposure to isoflurane induces learning and memory deficits of old rats. IL-1 beta in the hippocampus was increased at 4 h after isoflurane exposure. Isoflurane also increased neuroapoptosis in the hippocampus and decreased neuronal density in the CA1 region. And GTS-21 pretreatment effectively alleviated these changes. Conclusions: The study demonstrated that pretreatment with alpha 7 nicotinic acetylcholine receptor agonist GTS-21 attenuates isoflurane-induced learning and memory impairment in aged rats. (C) 2015 Elsevier Inc. All rights reserved.
引用
收藏
页码:255 / 261
页数:7
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