Acute spinal cord injury in rats induces autophagy activation.

AIM Autophagy is an important process that balances cellular protein synthesis and degradation and is involved in many physiological and pathological conditions. However, the precise role of autophagy has not yet been defined in the model of spinal cord injury (SCI). MATERIAL AND METHODS Here, we utilized a hemisection model of acute SCI to elucidate the role of autophagy in the pathological processes underlying SCI. RESULTS LC3B-II, a well-known marker of autophagy, was immunohistochemically detected 4H after SCI, peaked at 3D, and decreased at 21D. Hematoxylin-eosin (HE) staining confirmed accurate spinal cord hemisection, which was accompanied by both neuronal swelling and shrunken neurons with darkly stained, condensed nuclei. These findings suggest that the process of autophagy is related with pathological changes following SCI. CONCLUSION Our results indicate autophagy is involved in the pathological changes after SCI, and potential therapies to promote neuronal regeneration following SCI should target the mechanism of autophagy.