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Melatonin attenuates scopolamine-induced cognitive impairment via protecting against demyelination through BDNF-TrkB signaling in the mouse dentate gyrus
Chemico-Biological Interactions ( IF 5.1 ) Pub Date : 2018-02-21 , DOI: 10.1016/j.cbi.2018.02.023
Bai Hui Chen , Joon Ha Park , Tae-Kyeong Lee , Minah Song , Hyunjung Kim , Jae Chul Lee , Young-Myeong Kim , Choong-Hyun Lee , In Koo Hwang , Il Jun Kang , Bing Chun Yan , Moo-Ho Won , Ji Hyeon Ahn

Animal models of scopolamine-induced amnesia are widely used to study underlying mechanisms and treatment of cognitive impairment in neurodegenerative diseases such as Alzheimer's disease (AD). Previous studies have identified that melatonin improves cognitive dysfunction in animal models. In this study, using a mouse model of scopolamine-induced amnesia, we assessed spatial and short-term memory functions for 4 weeks, investigated the expression of myelin-basic protein (MBP) in the dentate gyrus, and examined whether melatonin and scopolamine cotreatment could keep cognitive function and MBP expression. In addition, to study functions of melatonin for keeping cognitive function and MBP expression, we examined expressions of brain-derived neurotrophic factor (BDNF) and tropomycin receptor kinase B (TrkB) in the mouse dentate gyrus. Scopolamine (1 mg/kg) and melatonin (10 mg/kg) were intraperitoneally treated for 2 and 4 weeks. Two and 4 weeks after scopolamine treatment, mice showed significant cognitive impairment; however, melatonin and scopolamine cotreatment recovered cognitive impairment. Two and 4 weeks of scopolamine treatment, the density of MBP immunoreactive myelinated nerve fibers was significantly decreased in the dentate gyrus; however, scopolamine and melatonin cotreatment significantly increased the scopolamine-induced reduction of MBP expression in the dentate gyrus. Furthermore, the cotreatment of scopolamine and melatonin significantly increased the scopolamine-induced decrease of BDNF and TrKB immunoreactivity in the dentate gyrus. Taken together, our results indicate that melatonin treatment exerts anti-amnesic effect and restores the scopolamine-induced reduction of MBP expression through increasing BDNF and TrkB expressions in the mouse dentate gyrus.



中文翻译:

褪黑素可通过防止鼠齿状回中的BDNF-TrkB信号转导脱髓鞘作用,减轻东pol碱引起的认知障碍

东sco碱引起的失忆症的动物模型被广泛用于研究神经退行性疾病如阿尔茨海默氏病(AD)的潜在机制和认知障碍的治疗。先前的研究已经确定褪黑激素可改善动物模型中的认知功能障碍。在这项研究中,使用东sco碱诱导的失忆症的小鼠模型,我们评估了4周的空间和短期记忆功能,调查了齿状回中髓鞘碱性蛋白(MBP)的表达,并检查了褪黑素和东pol碱是否同时治疗可以保持认知功能和MBP表达。此外,为了研究褪黑激素保持认知功能和MBP表达的功能,我们检查了小鼠齿状回中脑源性神经营养因子(BDNF)和原霉素受体激酶B(TrkB)的表达。腹膜内注射东co碱(1 mg / kg)和褪黑激素(10 mg / kg)2周和4周。东碱治疗后第2和第4周,小鼠表现出明显的认知障碍。然而,褪黑素和东pol碱共同治疗可以恢复认知障碍。东碱治疗第2和第4周,齿状回中MBP免疫反应性有髓神经纤维的密度显着降低。然而,东pol碱和褪黑激素的联合治疗显着增加了东pol碱诱导的齿状回中MBP表达的减少。此外,东pol碱和褪黑激素的共同治疗显着增加了东pol碱诱导的齿状回中BDNF和TrKB免疫反应性的降低。在一起

更新日期:2018-02-21
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