Sodium Butyrate Exerts Neuroprotective Effects in Spinal Cord Injury.

Abstract

Sodium butyrate (SB) is a dietary microbial fermentation product and serves as an important neuromodulator in the central nervous system. Recent experimental evidence has suggested potential therapeutic applications for butyrate, including its utility in treating metabolic and inflammatory diseases. The aim of the present study was to evaluate the potential beneficial effects of SB in a mouse model of spinal cord injury (SCI) and its possible mechanism of action. SCI was induced by extradural compression for 1min of the spinal cord at the T6-7 level using an aneurysm clip, and SB (10-30-100mg/kg) was administered by oral gavage 1 and 6 h after SCI. For locomotor activity, study mice were treated with SB once daily for 10days. Morphological examination was performed by light microscopy through hematoxylin-eosin (H&E) staining. In addition, NF-κB, IκB-α, COX-2, and iNOS expressions were assayed by western blot analysis and IL-1β and TNF-α levels by immunohistochemistry analysis. The results showed that SB treatment significantly ameliorated histopathology changes and improved recovery of motor function changes in spinal cord injury in a dose-dependent manner. Moreover, we demonstrated that SB modulated the NF-κB pathway showing a significant reduction in cytokine expression. Thus, this study showed that SB exerts neuroprotective effects anti-inflammatory properties following spinal cord injury suggesting that SB may serve as a potential candidate for future treatment of spinal cord injury.