Sodium butyrate (SB) is a dietary microbial fermentation product of dietary fiber 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 produced by extradural compression for 1 min of the spinal cord at the T6–7 level using an aneurysm clip, and SB (10–30–100mg/kg) were administered by oral gavage 1 and 6 h after SCI. For locomotor activity, study mice were treated with SB once daily for 10 days. Morphological examination was performed by light microscopy through hematoxylin‐eosin (H&E) staining. In addition, NF‐kB, IkB‐alfa, COX2 and iNOS expression were assayed by western blot analysis and IL‐1beta and TNF‐alfa 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 dose‐dependet manner. Moreover, from the results obtained, SB modulated NF‐kB pathway showing a reduction in cytokines expression. This study showed that SB exerts neuroprotective effects on spinal cord injury and anti‐inflammatory properties. The observed neuroprotective action suggests that SB may serve as a potential candidate for future treatment of spinal cord injury.Support or Funding InformationNo foundingThis abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.