Curcumin promotes functional recovery after spinal cord injury by enhancing autophagic flux and attenuating apoptosis.

AIM: This study aimed to investigate the neuroprotective effects of curcumin on apoptosis and autophagy regulation following spinal cord injury (SCI) in a rat model.

METHODS

Adult male rats were randomly assigned to three groups: sham, SCI, and SCI + curcumin (100 mg/kg/day, i.p. for 14 days). SCI was induced using a standardized contusion model at T9. Locomotor recovery was evaluated using the Basso, Beattie, and Bresnahan (BBB) score over 28 days post-injury. Histopathological assessment was performed on spinal cord sections using hematoxylin and eosin (H&E) and Nissl staining. Apoptosis was assessed using the TUNEL assay, counterstained with DAPI. Immunofluorescence staining for LC3 and p62 and Western blotting for LC3-I/II, Beclin-1, and p62 were used to evaluate autophagic responses.

RESULTS

Curcumin significantly improved locomotor function in SCI rats, as indicated by higher BBB scores. Histological analysis revealed reduced cavitation and preserved neuronal architecture in the SCI + curcumin group. The percentage of TUNEL-positive cells was significantly reduced in the curcumin-treated group (30.47 ± 10.41%) compared to the SCI group (68.75 ± 12.25%, p < 0.01). Curcumin treatment enhanced autophagic activity by increasing LC3 puncta and reducing p62 aggregates. Western blot data confirmed upregulation of Beclin-1 and LC3-II, restoration of LC3-I, and suppression of p62 expression.

CONCLUSION

Curcumin exerts neuroprotective effects following SCI, potentially by attenuating apoptosis within spinal tissue and enhancing autophagic flux through modulation of key regulatory markers. These findings suggest that curcumin may be a promising therapeutic agent for SCI treatment.