摘要
目的：神经炎症的病因仍然是不确定的，有效的干预措施来阻止神经退行性疾病仍然难以获得。令人惊讶的是，我们发现II型胶原结合完全弗氏佐剂（CC），通常能诱导小鼠产生类风湿关节炎（RA）也驱动阿尔茨海默氏症（AD）样神经退行性变。完全弗氏佐剂不仅上调大脑促炎性细胞因子包括肿瘤坏死因子（TNF-α）和白细胞介素8（IL-8），而且下调大脑中抗炎细胞因子白细胞介素10（IL-10）和抗炎递质多巴胺生物合成的限速酶酪氨酸羟化酶（TH）。相反，电针首先提高TNF-α/ IL-8水平，降低IL-10/TH水平，随后又可降低TNF-α/ IL-8水平，升高IL-10/TH水平。对线粒体的生物合成、泛素化和自噬的影响，EA首先控制然后削弱CC触发的信号转导通路从而导致氧化、亚硝基化、缺氧与血管生成。最终，EA通过降低淀粉样-β肽（Aβ）和磷酸化类tau蛋白（p-tau）来阻碍神经退行性变化，并通过增加胆碱能神经递质乙酰胆碱（ACh）及其限速合成酶胆碱乙酰基转移酶（ChAT）来改善神经功能障碍。 结果：总的来说，EA起初加重，随后改善CC诱发AD样早期脑机制从促炎小胶质细胞到抗炎小胶质细胞转换。
关键词: 阿尔茨海默病，电针，炎症性病变，炎症，神经退行性疾病，氧化应激
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