Effects of melatonin on cognitive impairment and hippocampal neuronal damage in a rat model of chronic cerebral hypoperfusion

被引：36

作者：

Lee, Choong Hyun ^{[1
]}

Park, Joon Ha ^{[2
]}

Ahn, Ji Hyeon ^{[2
]}

Won, Moo-Ho ^{[2
]}

机构：

[1] Dankook Univ, Coll Pharm, Dept Pharm, Cheonan 330714, Chungcheongnam, South Korea

[2] Kangwon Natl Univ, Sch Med, Dept Neurobiol, 192-1 Hyoja 2 Dong, Chunchon 200701, Gangwon, South Korea

来源：

EXPERIMENTAL AND THERAPEUTIC MEDICINE | 2016年 / 11卷 / 06期

基金：

新加坡国家研究基金会;

关键词：

melatonin; chronic cerebral hypoperfusion; spatial learning and memory; neuronal damage; microglial activation; pro-inflammatory cytokines; CHRONIC BRAIN HYPOPERFUSION; OXIDATIVE STRESS; MEMORY IMPAIRMENT; DYSFUNCTION; EXPRESSION; ISCHEMIA; DEFICITS; ACTIVATION; REDUCTION;

D O I：

10.3892/etm.2016.3216

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：

Chronic cerebral hypoperfusion (CCH), which induces oxidative stress and inflammation in the brain, has previously been associated with cognitive impairment and neuronal cell damage. Melatonin is a well-known free radical scavenger and antioxidant; therefore, the present study investigated the protective effects of melatonin against CCH-induced cognitive impairment and neuronal cell death in a CCH rat model, which was generated via permanent bilateral common carotid artery occlusion (2VO). The rats in the 2VO group exhibited markedly increased escape latencies in a Morris water maze test, as compared with the rats in the sham group. In addition, increased neuronal cell damage was detected in the hippocampal CA1 region of the 2VO rats, as compared with the rats in the sham group. Treatment of the 2VO rats with melatonin significantly reduced the escape latency and neuronal cell damage, and was associated with reduced levels of malondialdehyde, microglial activation, and tumor necrosis factor-alpha and interleukin-1 beta in the ischemic hippocampus. The results of the present study suggest that melatonin may attenuate CCH-induced cognitive impairment and hippocampal neuronal cell damage by decreasing oxidative stress, microglial activation and the production of pro-inflammatory cytokines in the ischemic hippocampus.

引用

页码：2240 / 2246

页数：7

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