电针通过抑制慢性轻度应激小鼠海马NF-κB/NLRP3炎症通路预防抑郁样行为

IF 2.3 4区 心理学 Q3 NEUROSCIENCES
Neuropsychobiology Pub Date : 2022-01-01 Epub Date: 2022-01-11 DOI:10.1159/000521185
Qi Wang, Hongsheng Bi, Hongfei Huang, Yitong Wang, Lili Gong, Na Qi, Dongdong Li, Xin Jin, Tianchao Xu, Baoguang Shi
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引用次数: 6

摘要

背景:针刺治疗抑郁症的确切生理机制尚不清楚。本研究旨在观察电针(EA)对慢性轻度应激(CMS)模型小鼠抑郁样行为的影响,并探讨其机制。方法:采用CMS方法建立抑郁模型,持续6周。在CMS模式的第三周后,在3周的时间内每天进行15分钟的EA治疗。采用蔗糖偏好试验和强迫游泳试验(FST)评价EA的抗抑郁样作用。检测小鼠海马组织核因子κB (NF-κB)、p-NF-κB、NF-κB抑制剂、p -κB α、nod样受体蛋白3、白细胞介素(IL)-6、IL-1β、IL-18、肿瘤坏死因子-α (TNF-α)的蛋白水平。结果:CMS治疗6周后,蔗糖偏好降低,EA可逆转CMS的作用。在FST试验中,CMS增加了固定时间,减少了第一次固定的潜伏期,但这些作用被EA逆转。CMS诱导NF-κB (NF-κB核/质比)进入核,海马中p-NF-κB和p- i -κB α蛋白水平升高。CMS还增加了海马中NLRP3的水平。此外,CMS可使海马组织中IL-6、IL-1β、IL-18、TNF-α水平升高,并可逆转应激作用。结论:EA可通过抑制NF-κB/NLRP3炎症通路抑制CMS诱导的抑郁样行为。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Electroacupuncture Prevents the Depression-Like Behavior by Inhibiting the NF-κB/NLRP3 Inflammatory Pathway in Hippocampus of Mice Subjected to Chronic Mild Stress.

Background: The precise physiological mechanisms of acupuncture in the treatment of depression are still unknown. This study aimed to observe the effects of electroacupuncture (EA) on depression-like behavior of mouse in chronic mild stress (CMS) model and explore the underlying mechanism.

Methods: The depression model was established by using CMS method for 6 weeks. After the third week of the CMS paradigm, EA treatment was performed daily for 15 min over a period of 3 weeks. The antidepressant-like effects of EA were evaluated using the sucrose preference test and the forced swimming test (FST). The protein levels of the nuclear factor-kappa B (NF-κB), p-NF-κB, inhibitor of NF-κB, p-IκBα, NOD-like receptor protein 3, interleukin (IL)-6, IL-1β, IL-18, and tumor necrosis factor-α (TNF-α) in hippocampus of mice were detected.

Results: Sucrose preference was decreased after 6 weeks of CMS and the effects of CMS was reversed by EA. CMS increased immobility time and decreased latency to the first immobility in the FST test, but these effects were reversed by EA. CMS-induced nuclear entry of NF-κB (nuclear/cytoplasmic ratio of NF-κB) with an increase in protein levels of p-NF-κB and p-IκBα in the hippocampus. The CMS also increased NLRP3 levels in the hippocampus. However, these effects were reversed by EA. In addition, the levels of IL-6, IL-1β, IL-18, and TNF-α in the hippocampus were increased by CMS, and these effects of stress were reversed by EA.

Conclusion: EA prevented CMS-induced depressive-like behaviors by inhibiting NF-κB/NLRP3 inflammatory pathway.

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来源期刊
Neuropsychobiology
Neuropsychobiology 医学-精神病学
CiteScore
7.20
自引率
0.00%
发文量
26
审稿时长
6 months
期刊介绍: The biological approach to mental disorders continues to yield innovative findings of clinical importance, particularly if methodologies are combined. This journal collects high quality empirical studies from various experimental and clinical approaches in the fields of Biological Psychiatry, Biological Psychology and Neuropsychology. It features original, clinical and basic research in the fields of neurophysiology and functional imaging, neuropharmacology and neurochemistry, neuroendocrinology and neuroimmunology, genetics and their relationships with normal psychology and psychopathology. In addition, the reader will find studies on animal models of mental disorders and therapeutic interventions, and pharmacoelectroencephalographic studies. Regular reviews report new methodologic approaches, and selected case reports provide hints for future research. ''Neuropsychobiology'' is a complete record of strategies and methodologies employed to study the biological basis of mental functions including their interactions with psychological and social factors.
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