Antidepressant effect of electroacupuncture on modulating the expression of c‐Fos/AP‐1 through the JNK signaling pathway. Issue 11 (25th August 2021)

• Record Type: Journal Article
• Authors: Li, Xiang; Qi, Si‐Min; Wang, Yu; Jiang, Hui‐Wu; Li, Ya‐Huan; Zhao, Bing‐Cong; Zhang, Tao; Sun, Yang; Gao, Xing‐Zhou; Quan, Song‐Xiao; Liu, Peng‐Fei; Li, Wen‐Shan; Wu, Ji‐Hong; Bao, Tu‐Ya; Jiang, Hui‐Li
• Is Part Of: Anatomical record. Volume 304:Issue 11(2021)
• Page Start: 2480
• Page End: 2493
• Publication Date: 2021-08-25
• Subjects: depression -- electroacupuncture -- JNK signaling pathway -- SP600125 -- stress; Anatomy -- Periodicals; Evolution (Biology) -- Periodicals; Morphology -- Periodicals; 571.3
• DOI: 10.1002/ar.24740
• Languages: English
• ISSNs: 1932-8486

Abstract

Abstract: The effectiveness and safety of electroacupuncture (EA) for depression have been identified by abundant clinical trials and experimental findings. The c‐Jun‐NH(2)‐terminal kinase (JNK) signaling pathway is considered to be involved in the antidepressant mechanism of EA. However, the antidepressant effect of EA via modulating the expression of c‐Fos/activator protein‐1 (AP‐1) under the condition of JNK inhibition remains unexplored. In this study, we investigated the antidepressant effect and possible mechanism of EA in regulating the expression of c‐Fos/AP‐1 under the condition of JNK inhibition by SP600125 in rats exposed to chronic unpredictable mild stress (CUMS). The depression‐like behaviors were evaluated by the body weight, sucrose preference test (SPT), and open field test (OFT). The expression levels of c‐Jun in the hypothalamus, c‐Fos in the pituitary gland, and c‐Fos and AP‐1 in the serum of CUMS induced rat model of depression were detected by ELISA. The results indicated that treatment with EA and fluoxetine can reverse the CUMS‐induced depression‐like behaviors in rats and can up‐regulate the expression levels of c‐Jun in the hypothalamus, c‐Fos in the pituitary gland, and c‐Fos and AP‐1 in the serum. Of note, the data demonstrated that SP600125, the inhibitor of JNK signaling pathway, can exert synergistic effect with EA in regulating CUMS‐induced abnormal activation of the JNK signaling pathway. The antidepressant effect of EA might be mediated by modulating the expression of c‐Fos/AP‐1. Abstract : 摘要: 目前电针抗抑郁的有效性和安全性得到大量临床研究和实验结果的证实，JNK信号通路被认为是参与了电针抗抑郁的机制过程。然而，电针通过在阻断JNK信号通路条件下调节c‐Fos/AP‐1表达的抗抑郁机制尚未阐明。在本研究中，我们主要探究电针通过SP600125抑制JNK信号通路条件下调节慢性温和不可预知性应激(CUMS)抑郁模型c‐Fos/AP‐1表达的抗抑郁效应机制。通过体重监测、糖水偏好实验和旷场实验评价抑郁样行为；采用酶联免疫吸附剂测定技术(ELISA)检测下丘脑c‐Jun、垂体c‐Fos及血清c‐Fos、AP‐1水平。结果显示，电针及氟西汀干预显著改善了CUMS诱导的大鼠抑郁样行为，并逆转了CUMS诱导的下丘脑水平c‐Jun、垂体c‐Fos及血清c‐Fos、AP‐1上调表达。值得注意的是，研究数据表明JNK信号通路特异性阻断剂SP600125同电针一起在调节CUMS诱导的JNK信号通路异常激活上起到协同作用，电针抗抑郁效应可能是通过调节应激诱导的c‐Fos/AP‐1表达介导的。