MiR-7a ameliorates spinal cord injury by inhibiting neuronal apoptosis and oxidative stress.

Abstract

The aim of this study was to investigate the therapeutic effect of microRNA-7a (miR-7a) on spinal cord injured rats and to explore its underlying mechanism in vivo. The spinal cord injury (SCI) model was first established in adult rats. The epicenter of the lesion was treated with miR-7a mimics via intrathecal injection. The Basso-Beattie-Bresnahan (BBB) locomotor rating scale was used to evaluate the functional recovery of hindlimbs in rats within 4 weeks following SCI. Western blotting and qPCR were utilized to detect the apoptosis and oxidative stress in rats treated with or without miR-7a. In addition, the neuron survival and neuro-filament amount were determined using immunofluorescence. After SCI and miR-7a treatment, the locomotor recovery of treated rats was significantly improved when compared with rats without treatment. The mitochondrial disorder and cell death were significantly reduced in miR-7a treated rats. Meanwhile, the nuclear transcription factor-κB (NF-κB) pathway was significantly reduced as well. Contrarily, the expression of anti-apoptotic protein Bcl-2 and NF-κB inhibitor I-κB was remarkably elevated in miR-7a treated rats. In addition, up-regulation of miR-7a rescued neurons and maintained the neural structure. The up-regulation of miR-7a alleviated the injury-induced oxidative stress and inhibited apoptosis by down-regulating NF-κB pathway in SCI rats.