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.