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 swimming test (FST). 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 corticosteronetreated 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.
Highlights
Major depression disorder (MDD) is one of the most common debilitating mood disorders worldwide and becoming the second leading disease contributing to the years lived with disability by 2013 (Dean and Keshavan, 2017)
The objective of this study was to verify the antidepressant-like effects of red wine phenolic extracts in a mouse model of depression induced by repeated injections of corticosterone, and to further investigate the relationship between brain-derived neurotrophic factor (BDNF) signaling and the antidepressant-like effect of red wine phenolic extracts
Post-hoc analysis revealed that long-term treatment of corticosterone mice with TPs extract (TPx)-MT7 (10, 20 mg/kg) increased sucrose preference, as compared to corticosterone-exposed mice
Summary
Major depression disorder (MDD) is one of the most common debilitating mood disorders worldwide and becoming the second leading disease contributing to the years lived with disability by 2013 (Dean and Keshavan, 2017). The prominent and persistent low mood, mental retardation, cognitive impairment, volitional decline and somatic symptoms companied the patients’ lifelong and impaired their social A growing literature has shown that the hypothalamic–pituitary–adrenal (HPA) axis plays a major role in the regulation of a variety of physiological disorders, such as depression (Menke, 2019) In this classic neuroendocrine circuit, limbic and hypothalamic brain structures coordinate emotional, cognitive, neuroendocrine and autonomic inputs, which together determine the magnitude and specificity of an individual’s behavioral, neural and hormonal responses to stress. Increased level of corticosterone has mostly been ascribed to impaired feedback regulation of the HPA axis, possibly caused by altered function of the glucocorticoid receptor and induced depressive disorder (Leistner and Menke, 2018)
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