Electroacupuncture Improves Memory and Protects Neurons by Regulation of the Autophagy Pathway in a Rat Model of Alzheimer—s Disease
| Autor: | Fang-fang Mou, Hai-dong Guo, Li-sheng Zhang, Shui-jin Shao, Guo-hong Cui, Xiao-jing Han, Yan-wu Xu, Jin-xin Tian, Jing Zhu, Da-yong Zhang, Zhi-hua Yu, Jiu-lin Chen |
|---|---|
| Rok vydání: | 2016 |
| Předmět: |
0301 basic medicine
Autophagosome medicine.medical_specialty Pathology Electroacupuncture medicine.medical_treatment Rat model Morris water navigation task Apoptosis Haematoxylin Hippocampus 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine Alzheimer Disease Memory Internal medicine Autophagy Animals Medicine Neurons Memory Disorders Amyloid beta-Peptides TUNEL assay business.industry Adenine General Medicine Peptide Fragments Rats Disease Models Animal 030104 developmental biology Endocrinology Complementary and alternative medicine chemistry Beclin-1 Neurology (clinical) business Microtubule-Associated Proteins 030217 neurology & neurosurgery |
| Zdroj: | Acupuncture in Medicine. 34:449-456 |
| ISSN: | 1759-9873 0964-5284 |
| DOI: | 10.1136/acupmed-2015-010894 |
| Popis: | Background Acupuncture is a potential therapy for Alzheimer's disease (AD), but its clinical effects and underlying mechanisms are not fully understood. Emerging evidence suggests autophagy is involved in β-amyloid (Aβ) clearance. We hypothesised that electroacupuncture (EA) treatment of AD involves the autophagy pathway in rats. Methods We injected 2μl Aβ1–40 bilaterally into the hippocampi of 42 rats to establish AD. Rats remained untreated (AD group, n=14) or received 24 EA treatments at GV20+BL23 over 28 days from day 7 post-injection with/without co-treatment with 3-methyladenine (3-MA), an autophagy inhibitor (AD+EA+3-MA and AD+EA groups, respectively, n=14 each). Cognitive function was evaluated by Morris water maze (MWM) testing. Hippocampi were examined by transmission electron microscopy (TEM) and stained with haematoxylin and eosin/transferase dUTP nick end labelling (TUNEL) to assess neuronal morphology/apoptosis, respectively. Protein expression of Beclin-1, LC3 and Aβ1-40 was examined. Results In the MWM test, the AD+EA group showed an improvement in parameters consistent with improved learning/memory compared to untreated AD rats, and 3-MA attenuated these effects. EA mitigated cellular apoptosis resulting from Aβ infusion in the CA1 region and enhanced LC3II/LC3I ratios and Beclin-1 expression. Numerous autophagosome precursors and enlarged autophagosomes were observed by TEM in the hippocampi of EA-treated rats. Reduced Aβ levels, and co-localisation of Aβ and LC3II, were observed following EA treatment by immunofluorescence staining. EA+3-MA treated rats had much higher TUNEL-positive neurons, lower LC3II/LC3I ratios and Beclin-1 expression, and elevated Aβ levels compared with EA alone. Conclusions EA reduces neuronal apoptosis, enhances degradation of Aβ, and improves learning/memory in AD rats by upregulating the autophagy pathway. |
| Databáze: | OpenAIRE |
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