胡艳,刘若兰,肖佳欢,等.电针对阿尔茨海默病大鼠海马突触可塑性及自噬相关蛋白的影响[J].中华物理医学与康复杂志,2020,42(11):961-966
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| 电针对阿尔茨海默病大鼠海马突触可塑性及自噬相关蛋白的影响 |
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| DOI：10.3760/cma.j.issn.0254-1424.2020.11.001 |
| 中文关键词: 电针 阿尔茨海默病 学习记忆 长时程增强 自噬 |
| 英文关键词: Alzheimer′s disease Electroacupuncture Learning and memory Long-term potentiation Autophagy |
| 基金项目:国家自然科学基金青年项目（81603696） |
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| 中文摘要: |
| 目的 观察电针对阿尔茨海默病(AD)模型大鼠海马区突触可塑性及自噬的影响，探讨电针改善AD认知功能障碍的相关机制。 方法 采用随机数字表法将30只健康雄性SD大鼠分为假手术组、模型组及电针组，通过向双侧海马CA1区注射Aβ1-42将模型组及电针组大鼠制成AD动物模型，假手术组同部位注射等量生理盐水。于造模成功后次日，电针组选取百会、双侧肾俞穴进行电针治疗，每次治疗20 min，每天治疗1次，每周治疗6次，连续治疗2周。于治疗结束后采用Morris 水迷宫检测各组大鼠学习记忆能力，采用MED64微电极阵列检测大鼠海马区长时程增强（LTP）变化，采用透射电镜观察海马区自噬小体形成情况，采用Western Blot法检测海马区自噬相关蛋白1（Beclin-1）及微管相关蛋白轻链3（LC3）含量。 结果 与模型组比较，电针组大鼠逃避潜伏期明显缩短（P<0.05），穿越平台次数显著增多（P<0.05）；电针组大鼠海马区神经元兴奋性突触后电位波幅百分比较模型组显著增高（P<0.05）；模型组大鼠海马神经元中有大量自噬体，而电针组明显减少；电针组大鼠海马组织LC3Ⅱ/LC3I比值和Beclin-1蛋白表达量均较模型组显著降低（P＜0.05）。 结论 电针百会、肾俞穴可改善AD模型大鼠学习记忆功能，促进海马LTP恢复，其治疗机制可能与调控海马神经细胞自噬水平有关。 |
| 英文摘要: |
| Objective To investigate the effect of electroacupuncture (EA) on synaptic plasticity and the expression of autophagy-related proteins in the hippocampus in Alzheimer′s disease (AD). To explore how EA might improve cognition in AD. Methods Healthy male Sprague-Dawley rats were randomly divided into a sham operation group, a model group and an EA group. The rat model of AD was established by injecting Aβ1-42 into the bilateral CA1 area of the hippocampus. The sham operation group was injected with an equal amount of normal saline at the same site. Starting the day after the successful modelling, the EA group received 20 minutes of EA treatment at the Baihui (DU20) and bilateral Shenshu (BL23) acupoints once a day, 6 times a week for 2 weeks. The rats′ learning and memory were then tested using a Morris water maze. The long-term potentiation (LEP) in the hippocampus was assessed using a MED64 microelectrode array and any ultrastructural changes of autophagosomes were detected using an electron microscope. The expression of the autophagy-related proteins Beclin-1 and microtubule associated protein light chain 3 (LC3) in the hippocampus were determined using western blotting. Results The escape latency was significantly shorter and the times crossing the platform increased significantly in the EA group compared with the model group. The average amplitude of the postsynaptic excitatory field potentials in the EA group was significantly higher than among the model group. There were many autophagosomes in the hippocampal neurons of the model group, significantly more than in the EA group. The LC3II/LC3I ratio and Beclin-1 protein expression decreased significantly in the EA group compared to the model group. Conclusions EA can improve learning and memory and restore LEP in the hippocampus of rats modeling AD. The mechanism may be related to its regulation of autophagy in hippocampal neurons. |
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