Depression is a common disease that afflicts one in 6 people. Numerous hypotheses have been raised in the past decades, but the exact mechanism for depression onset remains obscure. Recently, the neuroinflammatory response and oxidative stress are being attracted more and more attention due to their roles in depression pathogenesis. The inhibition of neuroinflammatory response and oxidative stress is now considered a potential strategy for depression prevention and/or therapy. Sodium butyrate (SB) is a sodium form of the endogenous butyrate. It can inhibit proinflammatory responses and oxidative stress in different models of disease. In the present study, we investigated the effect of SB on lipopolysaccharide (LPS)-induced depression-like behaviors, neuroinflammatory response, and oxido-nitrosative stress in the hippocampus and prefrontal cortex in C57BL6/J mice. Our results showed that 10 days of SB pretreatment at the dose of 300 but not 100 mg/kg markedly ameliorated LPS (0.83 mg/kg)-induced depression-like behaviors in the tail suspension test, forced swimming test, and sucrose preference test. Further analysis showed that 10 days of SB pretreatment not only prevented LPS-induced increases in proinflammatory cytokines, such as interleukin (IL)-1β, IL-6, and tumor necrosis factor-α, in the hippocampus and prefrontal cortex but also prevented LPS-induced enhancement of oxido-nitrosative stress. Taken together, these results demonstrate that SB is such an agent that could be used to prevent depression onset and/or progression, and inhibition of neuroinflammatory response and oxido-nitrosative stress may be a potential mechanism for its antidepressant actions.
© 2020 S. Karger AG, Basel.

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