Sodium butyrate activates the K channels to regulate the mechanism of Parkinson's disease microglia model inflammation.

BACKGROUND

Parkinson's disease (PD) is a common neurodegenerative disorder. Microglia-mediated neuroinflammation has emerged as an involving mechanism at the initiation and development of PD. Activation of adenosine triphosphate (ATP)-sensitive potassium (K ) channels can protect dopaminergic neurons from damage. Sodium butyrate (NaB) shows anti-inflammatory and neuroprotective effects in some animal models of brain injury and regulates the K channels in islet β cells. In this study, we aimed to verify the anti-inflammatory effect of NaB on PD and further explored potential molecular mechanisms.

METHODS

We established an in vitro PD model in BV2 cells using 1-methyl-4-phenylpyridinium (MPP ). The effects of MPP and NaB on BV2 cell viability were detected by cell counting kit-8 assays. The morphology of BV2 cells with or without MPP treatment was imaged via an optical microscope. The expression of Iba-1 was examined by the immunofluorescence staining. The intracellular ATP content was estimated through the colorimetric method, and Griess assay was conducted to measure the nitric oxide production. The expression levels of pro-inflammatory cytokines and K channel subunits were evaluated by reverse transcription-quantitative polymerase chain reaction and western blot analysis.

RESULTS

NaB (5 mM) activated the K channels through elevating Kir6.1 and Kir6.1 expression in MPP -challenged BV2 cells. Both NaB and pinacidil (a K opener) suppressed the MPP -induced activation of BV2 cells and reduced the production of nitrite and pro-inflammatory cytokines in MPP -challenged BV2 cells.

CONCLUSION

NaB treatment alleviates the MPP -induced inflammatory responses in microglia via activation of K channels.