Electroacupuncture enhances the effects of escitalopram oxalate on glucocorticoid-inducible genes, inflammation and neurotrophin in depressed patients

BACKGROUND AND AIM: Evidence proved that electroacupuncture (EA) combined with antidepressants can improve the antidepressant effectiveness for depressed patients. However, the clinical mechanisms of EA remain unclear. This study aimed to observe the mechanism of EA as an adjunct therapy to escitalopram oxalate (EO) on depressed patients. EXPERIMENTAL PROCEDURE: This study was designed as a single‐blinded, double‐dummy randomized controlled trial. 61 participants were diagnosed with mild‐to‐moderate depression according to the International Classification of Diseases 10th Edition (ICD‐10, F32) were randomly allocated to receive EA + EO placebo, EO + sham EA, or EA + EO for six weeks treatment. The clinical assessment including depression severity, quality of life (QOL) and clinical safety. Biological indicators of immune‐inflammation, the brain‐derived neurotrophic factor and glucocorticoid inducible genes in peripheral blood of participants were measured by using enzyme linked immunosorbent assay and real‐time polymerase chain reaction respectively before and after treatment. RESULTS AND CONCLUSION: Three interventions improved the depression severity and QOL (P < 0.05), and no inter‐group difference was found in the 6th week (P > 0.05). Anxiety psychic and somatic general symptoms in the EA + EO group were improved significantly than those of the other two groups (P < 0.05). After six‐week treatment of EA + EO, blood SGK1 mRNA, GILZ mRNA, and BDNF levels were increased significantly (P < 0.05), and IL‐6 levels were decreased significantly (P < 0.05) in depressed patients. IL‐6 change levels were positively correlated with the change of HAMD‐24 score in patients who received EA + EO treatment (P < 0.05). EA as an add‐on therapy of EO probably enhanced antidepressant effectiveness through regulating multiple targets involved in blood BDNF, IL‐6, and glucocorticoid‐inducible genes GILZ mRNA and SGK‐1 mRNA.