Abstract
Depression is an inflammatory-related condition, with the progression in neuronal damage resulting in major depression disorder. Ginsenoside-Rg1, a sterol extract from the herb Panax ginseng, has been shown to exert neuroprotective effects upon neurodegeneration disorders. However, whether ginsenoside-Rg1 confers antidepressant-like effects on neuroinflammation as associated with depression, as well as the possible mechanism involved in these neuroprotective effects, is currently unclear. In the present report, we show that treatment with ginsenoside-Rg1 (40 mg/kg, i.p.) significantly ameliorated depressive-like behaviors as induced by chronic unpredictable mild stress (CUMS) in a rat model of depression. Moreover, these CUMS rats treated with ginsenoside-Rg1 showed reductions in the levels of the oxidative stress products and the activity in the antioxidant stress kinase. Furthermore, CUMS rats treated with ginsenoside-Rg1 showed ameliorated neuroinflammation and associated neuronal apoptosis along with a reduction in dendritic spine atrophy and display of depressive behaviors. Taken together, the results of this study suggest that ginsenoside-Rg1 produces antidepressant-like effects in CUMS-exposed rats; and one of the mechanisms for these antidepressant-like effects of ginsenoside-Rg1 appears to involve protection against oxidative stress and thus the neuronal deterioration resulting from inflammatory responses. These findings provide evidence for the therapeutic potential of ginsenoside-Rg1 in the treatment of stress-related depression.
Highlights
Depression is considered a pervasive, worldwide neuropsychological disease associated with enormous medical and economic burdens on individuals and society [1]
Ginsenoside-Rg1 treatment effectively alleviated this behavioral despair as indicated by decreased immobility and increased swimming durations in chronic unpredictable mild stress (CUMS) rats (P < 0:05, for both)
There was no significant difference between the ginsenoside-Rg1-treated nonstressed control group and the nonstressed control group (P > 0:05)
Summary
Depression is considered a pervasive, worldwide neuropsychological disease associated with enormous medical and economic burdens on individuals and society [1]. Within studies using animal models of depression, significant elevations in some critical proinflammatory cytokines including interleukin-1β (IL-1β), interferon-γ (IFN-γ), and tumor necrosis factor-α (TNF-α) were present, whereas treatments with some putative antidepressant drugs or neuroprotective reagents reduced the levels of these proinflammatory cytokines to varying degrees while producing antidepressant-like effects [10, 11]. These results provide strong evidence indicating that inflammationinduced neuronal injury may represent a major risk factor for the development of depression. Targeting relevant neuronal mechanisms underlying this inflammation-induced pathogenesis of depression progression has the potential to serve as both a novel therapeutic and preventative approach in the treatment of this disorder
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