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电针对 AD 模型大鼠的神经细胞凋亡具有抑制作用,并能改善认知功能障碍,其作用机制可能与下调 Notch 信号通路有关。

Electroacupuncture Suppressed Neuronal Apoptosis and Improved Cognitive Impairment in the AD Model Rats Possibly via Downregulation of Notch Signaling Pathway.

机构信息

Department of Anatomy, School of Basic Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, China.

Department of Endocrinology, The People's Hospital of Zhangqiu, Shandong 250200, China.

出版信息

Evid Based Complement Alternat Med. 2015;2015:393569. doi: 10.1155/2015/393569. Epub 2015 Feb 25.

DOI:10.1155/2015/393569
PMID:25810743
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4355557/
Abstract

Acupuncture is a potential strategy for the treatment of Alzheimer's disease (AD) and the possible mechanisms worth to be explored. In this study, we proposed and tested the hypothesis that whether Notch signaling pathway is involved in the effect of electroacupuncture (EA) treatment. Rats that received EA treatment on the acupoints of Baihui (Du 20) and Shenshu (BL 23) had shorter latency and remained in the original platform quadrant longer and crossed the former platform contained quadrant more frequently compared to the Aβ injection rats without EA treatment. EA obviously alleviated the cell apoptosis resulted by Aβ infusion in hippocampus CA1 regions through upregulating the expression of Bcl-2 and downregulating the expression of Bax. EA could further obviously promote the expression of synapsin-1 and synaptophysin in hippocampus. Aβ injection significantly increased the expression of Notch1, Jag1, and Hes1 mRNA, while EA treatment downregulated the level of Notch1 and Hes1 mRNA in hippocampus, but not Jag1 mRNA. Our data suggested that EA treatment improved learning and memory function in the AD rat model partially through downregulating Notch signaling pathway.

摘要

针灸可能是治疗阿尔茨海默病(AD)的一种策略,值得探索其可能的机制。在这项研究中,我们提出并验证了以下假设:Notch 信号通路是否参与电针(EA)治疗的效果。与未接受 EA 治疗的 Aβ 注射大鼠相比,接受百会(Du 20)和肾俞(BL 23)穴位 EA 治疗的大鼠潜伏期更短,在原平台象限停留时间更长,穿过原平台包含象限的次数更多。EA 通过上调 Bcl-2 表达和下调 Bax 表达,明显减轻 Aβ 灌注引起的海马 CA1 区细胞凋亡。EA 可进一步明显促进海马突触素-1 和突触小体蛋白的表达。Aβ 注射显著增加了 Notch1、Jag1 和 Hes1 mRNA 的表达,而 EA 治疗下调了海马 Notch1 和 Hes1 mRNA 的水平,但 Jag1 mRNA 没有变化。我们的数据表明,EA 治疗通过下调 Notch 信号通路部分改善了 AD 大鼠模型的学习记忆功能。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f1b/4355557/d83a45d68f7b/ECAM2015-393569.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f1b/4355557/899f03c86781/ECAM2015-393569.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f1b/4355557/e2bdf19fc289/ECAM2015-393569.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f1b/4355557/9d9e53518c16/ECAM2015-393569.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f1b/4355557/d83a45d68f7b/ECAM2015-393569.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f1b/4355557/899f03c86781/ECAM2015-393569.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f1b/4355557/e2bdf19fc289/ECAM2015-393569.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f1b/4355557/9d9e53518c16/ECAM2015-393569.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f1b/4355557/d83a45d68f7b/ECAM2015-393569.004.jpg

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microRNA-9 attenuates amyloidβ-induced synaptotoxicity by targeting calcium/calmodulin-dependent protein kinase kinase 2.
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