Abstract: Spinal cord injury (SCI) causes motor, sensory and autonomic dysfunctions. The gut microbiome has an important role in SCI, while short chain fatty acids (SCFAs) are one of the main bioactive mediators of microbiota. In the present study, we explored the effects of oral administration of exogenous SCFAs on the recovery of locomotor function and tissue repair in SCI. Allen’s method was utilized to establish an SCI model in Sprague–Dawley (SD) rats. The animals received water containing a mixture of 150 mM SCFAs after SCI. After 21 days of treatment, the Basso, Beattie and Bresnahan (BBB) scores increased, the regularity index improved, and the BOS value declined. Spinal cord tissue inflammatory infiltration was alleviated, the spinal cord necrosis cavity was reduced, and the number of motor neurons and Nissl bodies was elevated. ELISA, RT-PCR and immunohistochemistry assays revealed that the expression of IL-10 increased and that of IL-17 decreased in the spinal cord. SCFAs promoted gut homeostasis, induced intestinal T cells to shift toward an anti-inflammatory phenotype, promoted regulatory T (Treg) cells to secrete IL-10, affecting Treg cells and IL-17⁺γδ T cells in the spinal cord. Furthermore, we observed that Treg cells migrated from the gut to the spinal cord region after SCI. The above findings confirm that SCFAs can regulate Treg cells in the gut and affect the balance of Treg and IL-17⁺γδ T cells in the spinal cord, which inhibit the inflammatory response and promote the motor function in SCI rats. Our findings suggest that there is a relationship between gut, spinal cord and immune cells, and the "gut-spinal cord-immune" axis may be one of the mechanisms regulating neural repair after SCI.