Inhibition of miR-214-5p attenuates inflammatory chemotaxis and nerve regeneration obstruction after spinal cord injury in rats

P. Wang, Z.-W. Li, Z. Zhu, Z.-Y. Zhang, J. Liu

Department of Neurology, the Second Hospital of Jilin University, Changchun, China. 51723558@qq.com

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• Orthopedics

OBJECTIVE: To investigate the effect of miR-214-5p on spinal cord injury (SCI) and the possible mechanism in pathophysiological relevance, and to evaluate the therapeutic efficacy of the corresponding inhibitor.

MATERIALS AND METHODS: The SCI model was successfully established in 6-week-old rats. The levels of locomotor function recovery in rats of miR-214-5p inhibitor group and SCI group were detected one month later by Basso-Beattie-Bresnahan (BBB) locomotor rating scale, Western blotting, quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) and enzyme-linked immunosorbent assay (ELISA), respectively. Rat microglia cells were cultured in vitro. Furthermore, the effect of miR-214-5p and its inhibitor on inflammatory microglia was explored.

RESULTS: Compared with SCI group, rats in miR-214-5p inhibitor group showed a significant retardation of inflammatory diffusion in terms of reduced production of inflammatory factors and chemokines in vivo. MiR-214-5p inhibitor markedly attenuated antioxidant stress, inhibited apoptosis, and increased nerve fibers repair. Compared with lipopolysaccharide (LPS) group, tumor necrosis factor alpha (TNF-α) and interleukin 1 (IL-1) decreased significantly in microglia treated with miR-214-5p inhibitor in vitro. Furthermore, inhibition of miR-214-5p remarkably promoted locomotor function recovery in rats.

CONCLUSIONS: MiR-214-5p inhibitor retarded inflammatory diffusion by inhibiting inflammatory factors and chemokines after SCI. In addition, this might relieve nerve structure destruction, resist oxidative stress and inhibit apoptosis, eventually promoting function recovery.

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