Autophagy is confirmed to be involved in the onset and development of depression, and some antidepressants took effect by influencing the autophagic process. Electroacupuncture (EA), as a common complementary treatment for depression, may share the mechanism of influencing autophagy in the hippocampus like antidepressants. To investigate that, sixty Sprague-Dawley rats firstly went through chronic unpredictable mild stress (CUMS) model establishment, and 15 rats were assigned to a control group. After modeling, 45 successfully CUMS-induced rats were randomly divided to 3 groups: CUMS, selective serotonin reuptake inhibitor (SSRI), and EA groups (15 rats per group), to accept different interventions for 2 weeks. A sucrose preference test (SPT), weighing, and open field test (OFT) were measurement for depressive behaviors of rats. Transmission electron microscope (TEM), immunohistochemistry (IHC), and western blot analysis were used to evaluate the autophagic changes. After that, depression-like behaviors were successfully induced in CUMS models and reversed by SSRI and EA treatments (both ), but these two therapies had nonsignificant difference between each other (). Autolysosomes observed through TEM in the CUMS group were more than that in the control group. Their number and size in the SSRI and EA groups also decreased significantly. From IHC, the CUMS group showed enhanced positive expression of both Beclin1 and LC3 in CA1 after modeling (), and the LC3 level declined after EA treatments, which was verified by decreased LC3-II/LC3-I in western blot analysis. We speculated that CUMS-induced depression-like behavior was interacted with an autophagy process in the hippocampus, and EA demonstrated antidepressant effects by partly inhibiting autophagy with a decreased number of autolysosomes and level of LC3 along with LC3-II/LC3-I.

中文翻译：

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EA 改善了 CUMS 大鼠的抑郁行为并与其抑制海马自噬有关

自噬被证实参与了抑郁症的发生和发展，一些抗抑郁药通过影响自噬过程而发挥作用。电针（EA）作为一种常见的抑郁症辅助疗法，可能与抗抑郁药一样具有影响海马体自噬的机制。为了研究这一点，60 只 Sprague-Dawley 大鼠首先进行了慢性不可预测轻度应激 (CUMS) 模型的建立，并将 15 只大鼠分配到对照组。造模成功的45只CUMS诱导大鼠随机分为3组：CUMS组、选择性5-羟色胺再摄取抑制剂（SSRI）组和电针组（每组15只），接受不同的干预2周。蔗糖偏好试验（SPT）、称重和旷场试验（OFT）是对大鼠抑郁行为的测量。透射电子显微镜（TEM）、免疫组织化学（IHC）和蛋白质印迹分析用于评估自噬变化。之后，在 CUMS 模型中成功诱导了抑郁样行为，并通过 SSRI 和 EA 治疗（两者都是)，但是这两种疗法彼此之间没有显着差异（）。CUMS组透射电镜观察到的自溶酶体多于对照组。它们在 SSRI 和 EA 组中的数量和大小也显着减少。从 IHC 来看，CUMS 组在建模后显示 CA1 中 Beclin1 和 LC3 的阳性表达增强。)，并且电针处理后 LC3 水平下降，这通过蛋白质印迹分析中 LC3-II/LC3-I 的降低得到证实。我们推测 CUMS 诱导的抑郁样行为与海马中的自噬过程相互作用，并且 EA 通过减少自噬和 LC3-II/LC3-I 的数量和 LC3 水平来部分抑制自噬，从而表现出抗抑郁作用。