The aim of the study was to investigate the mechanism of microRNA (miR)-146a-mediated activation of interleukin-6/signal transducer and activator of transcription 3 (IL-6/STAT3) in lumbar intervertebral disc degeneration. To obtain intervertebral tissue, we recruited 5 patients with lumbar intervertebral disc herniation (experimental group) and 5 patients with lumbar burst fracture (control group). Nucleus pulposus tissue was extracted by surgery and cultured. miR-146a empty vector, mimic, and inhibitor were transfected into the two groups of cells for 24 h and the levels of IL-6, type II collagen (Col II), aggrecan, STAT3, matrix metalloproteinase (MMP)-3, and a disintegrin and metalloproteinase with thrombospondin type I motifs (ADAMTS) were detected. We found no differences in the levels of IL-6, Col II, aggrecan, STAT3, MMP-3, and ADAMTS before and after treatment in the control group. However, the levels of miR-146a, IL-6, STAT3, MMP-3, and ADAMTS were significantly elevated, whereas Col II and aggrecan levels were lower in the experimental group before treatment. The levels of IL-6, STAT3, MMP-3, and ADAMTS were elevated after treatment with miR-146a mimic when compared with the miR-146a empty vector in the experimental group, and Col II and aggrecan levels were decreased. However, the cells treated with miR-146a inhibitor had the opposite result. Thus, the IL-6/STAT3 signaling pathway can be mediated by a high expression of miR-146a to regulate the occurrence of lumbar intervertebral disc degeneration.
Keywords: Col II; a disintegrin and metalloproteinase with thrombospondin type I motifs; aggrecan; interleukin-6/signal transducer and activator of transcription 3 signaling pathway; lumbar intervertebral disc degeneration; matrix metalloproteinase; microRNA-146a.