MiRNA-411 attenuates inflammatory damage and apoptosis following spinal cord injury.

Abstract

To investigate the role and regulate the target of miRNA-411 on spinal cord injury. The microglia cultured in vitro was activated by lipopolysaccharide (LPS) to express the inflammatory phenotype. The inflammatory response through miRNA-411 transfection in microglia was measured to certain whether increased miRNA-411 suppressed interleukin-18 (IL-18) level to attenuate the inflammation amplification via downregulating JNK pathway. Furthermore, we established spinal cord injury (SCI) model in SD rats and further explored the glial inflammatory degree and neurological recovery following miRNA-411 treatment. Lastly, we estimated the hindlimbs function of SCI rats with miRNA-411 administration or not within four weeks at post-SCI. In vitro, miRNA-411 inhibited IL-18 expression and downregulated JNK pathway, along with that inflammatory microglia were declined. In SCI rats, we detected the decreased amounts of inflammatory microglia and reduction of the inflammatory factors after miRNA-411 treatment. IL-18 and JNK pathway was also restrained resulted from increased miRNA-411. In addition, apoptosis degree in injury site reduced and survived axons were relatively multiple in the miRNA-411 group compared with the SCI group. The Basso-Beattie-Bresnahan (BBB) locomotor scores of miRNA-411 treated rats were superior to those in rats with no treatment. MiRNA-411 increase ameliorates the inflammatory microglia-induced neurological lesion and promotes neural recovery by JNK pathway inhibition via negative targeting IL-18 in SCI.