Abstract
Previous studies have shown that lncRNA NEAT1 and miR-29b are closely associated with repair of the injured spinal cord. However, the mechanism by which lncRNA NEAT1 promotes regeneration after spinal cord injury by regulating miR-29b has not been reported. To explore this mechanism, we established a rat model of spinal cord injury (SCI). The experimental rats were randomly assigned to one of six groups: the sham, model, si-NEAT1, miR-29b, si-NEAT1 + negative control and si-NEAT1 + si-miR-29b groups. The hind limb motor function of the rats was evaluated on days 1, 3, 7, 14, and 21 after modelling using the BBB rating scale. Seven days after the operation, attenuation of pathological changes in injured spinal cord tissues was evaluated by HE staining. Anterior horn neurons and cavities in the injured area were counted by Nissl staining. In addition, the TUNEL assay was employed to study neuronal apoptosis in the anterior horn, and the expression of the apoptotic proteins Bcl-2 and Bax was analysed by western blotting. Finally, the protein expression of GFAP, NCAM, GAP43, and SCG10 was measured by immunohistochemistry and western blotting. BBB scores revealed that decreasing the level of NEAT1 improved the hind limb motor function of the rats by increasing miR-29b expression. H&E and Nissl staining showed that silencing NEAT1 attenuated lesions in the spinal cord and decreased the number of cavities in the injured spinal cord by upregulating miR-29b. Immunohistochemistry and western blotting suggested that silencing NEAT1 significantly downregulated GFAP expression and upregulated GAP43, SCG10 and NCAM expression by inducing overexpression of miR-29b. The TUNEL assay and western blotting also showed that silencing NEAT1 attenuated neuronal apoptosis.