Antidepressant effect of electroacupuncture on modulating the expression of c‐Fos/AP‐1 through the JNK signaling pathway

AbstractThe 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.