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电针对 APP/PS1 转基因小鼠的认知障碍具有改善作用,并能促进神经发生。

Electroacupuncture decreases cognitive impairment and promotes neurogenesis in the APP/PS1 transgenic mice.

机构信息

Department of Anesthesiology, Xijing Hospital, The Fourth Military Medical University, Xi'an 710032, Shaanxi Province, China.

出版信息

BMC Complement Altern Med. 2014 Jan 22;14:37. doi: 10.1186/1472-6882-14-37.

Abstract

BACKGROUND

Alzheimer's disease (AD) is a severe neurodegenerative disease for which there is currently no effective treatment. The purpose of this study was to investigate whether repeated electroacupuncture (EA) stimulation would improve cognitive function and the pathological features of AD in amyloid precursor protein (APP)/presenilin 1 (PS1) double transgenic mice.

METHODS

Cognitive function of APP/PS1 double transgenic mice was assessed using the Morris water maze test before and after EA treatment. Levels of amyloid β-peptide (Aβ) deposits in the hippocampus and cortex were evaluated by immunofluorescence, western blot and enzyme-linked immunosorbent assay. Expression of brain-derived neurotrophic factor (BDNF) was also examined by immunofluorescence and western blot. The neurogenesis was labeled by the DNA marker bromodeoxyuridine.

RESULTS

EA stimulation significantly ameliorated the learning and memory deficits of AD mice by shortening escape latency and increasing the time spent in the target zone during the probe test. Additionally, decreased Aβ deposits and increased BDNF expression and neurogenesis in the hippocampus and cortex of EA-treated AD mice were detected. The same change was detected in wild-type mice after EA treatment compared with wild-type mice without EA treatment.

CONCLUSIONS

Repeated EA stimulation may improve cognitive function, attenuate Aβ deposits, up-regulate the expression of BDNF and promote neurogenesis in the APP/PS1 double transgenic mice. This suggests that EA may be a promising treatment for AD.

摘要

背景

阿尔茨海默病(AD)是一种严重的神经退行性疾病,目前尚无有效的治疗方法。本研究旨在探讨重复电针(EA)刺激是否会改善 APP/PS1 双转基因小鼠的认知功能和 AD 的病理特征。

方法

在 EA 治疗前后,使用 Morris 水迷宫测试评估 APP/PS1 双转基因小鼠的认知功能。通过免疫荧光、western blot 和酶联免疫吸附试验评估海马和皮质中淀粉样β肽(Aβ)沉积水平。通过免疫荧光和 western blot 检测脑源性神经营养因子(BDNF)的表达。通过 DNA 标记物溴脱氧尿苷标记神经发生。

结果

EA 刺激显著改善了 AD 小鼠的学习和记忆缺陷,缩短了逃避潜伏期,并增加了探针测试中在目标区域的时间。此外,在 EA 治疗的 AD 小鼠的海马和皮质中检测到 Aβ 沉积减少,BDNF 表达增加和神经发生增加。与未经 EA 治疗的野生型小鼠相比,EA 治疗后的野生型小鼠也出现了相同的变化。

结论

重复 EA 刺激可能改善 APP/PS1 双转基因小鼠的认知功能,减轻 Aβ 沉积,上调 BDNF 的表达并促进神经发生。这表明 EA 可能是 AD 的一种有前途的治疗方法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3120/3907495/9daa25a968cb/1472-6882-14-37-1.jpg

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