Antidepressant-like activity of red wine phenolic extracts in repeated corticosterone-induced depression mice via BDNF/TrkB/CREB signaling pathway

¹ School of Functional Food and Wine,Shenyang Pharmaceutical University, Wenhua Road 103, Shenyang, PR China
² Seoul National University
³ School of Traditional Chinese Materia Medica, Shenyang Pharmaceutical University, Wenhua Road 103, Shenyang, PR China
⁴ The Engineering Laboratory of National and Local Union of Quality Control for Traditional Chinese Medicine, School of Pharmacy, Shenyang Pharmaceutical University, Wenhua Road 103, Shenyang 110016, China
⁵ School of Pharmaceutical Engineering, Shenyang Pharmaceutical University, Wenhua Road 103, Shenyang 110016, China
⁶ Polo Dois Portos, Instituto Nacional de Investigacao Agraria e Veterinaria, I.P., Quinta da Almoinha, 2565-191 Dois Portos, Portugal

^a e-mail: sun.baoshan@iniav.pt

Abstract

The aim of this study was to investigate the antidepressant-like effect of red wine phenolic extracts in mouse model exposed to exogenous corticosterone. The results showed that 3-week corticosterone injections caused depression-like behavior in mice, as indicated by the significant decrease in sucrose consumption and increase immobility time in the forced swim test. Red wine phenolic extracts treatment significantly reduced serum corticosterone levels. Moreover, it was found that red wine phenolic extract increased the brain-derived neurotrophic factor protein (BNDF) and Tropomyosin-related kinase B (TrkB) phosphorylation and cAMP-responsive element binding protein (CREB) phosphorylation levels in the hippocampus and prefrontal cortex. However, K252a, an inhibitor of TrkB, completely abolished those antidepressant-like effects. These results suggested that the red wine phenolic extracts produce an antidepressant-like effect in corticosterone-treated mice, at least in part, which is possibly mediated by modulating hypothalamic-pituitary-adrenal (HPA) axis, BDNF, TrkB and CREB phosphorylation levels in the brain region of mice.