Abstract: BACKGROUND: Pain mechanisms in patients with lumbar disc herniation are associated with inflammation, autophagy is closely related to intervertebral disc diseases and inflammatory response, and aberrant miR-206 expression can trigger skeletal diseases.
OBJECTIVE: To investigate the mechanism of miR-206 on inflammation, analgesia and autophagy related proteins in nucleus pulposus in rats with lumbar disc herniation. 
METHODS: Sixty SPF male Sprague-Dawley rats were randomly divided into control group, model group, miR-206 mimics-NC group, miR-206 mimics group, miR-206 inhibitor-NC group and miR-206 inhibitor group. Animal models of lumbar disc herniation were established except for the control group. Ten days after modeling, miR-206 mimics-NC group, miR-206 mimics group, miR-206 inhibitor-NC group and miR-206 inhibitor group were injected with miR-206 mimics-NC (20 μmol/L, 10 μL), miR-206 mimics (20 μmol/L, 10 μL), miR-206 inhibitor-NC (20 μmol/L, 10 μL) and miR-206 inhibitor (20 μmol/L, 10 μL), respectively. Administration was given once a day for 4 continuous days. The control group and model group were injected with the same dose of normal saline. The paw withdrawal mechanical threshold of bilateral hind feet was measured by Von Frey filaments, and the paw withdrawal thermal latency of bilateral hind feet was measured by heat pain tester. The morphology of dorsal root ganglia was observed by hematoxylin-eosin staining. The expressions of inflammatory factors phospholipase A2, cyclooxygenase 2, prostaglandin E2, tumor necrosis factor α, and interleukin 1β in nucleus pulposus were detected by qPCR. The expressions of autophagy-related proteins LC3I and Beclin-1 were detected by western blot assay. 
RESULTS AND CONCLUSION: At 3, 7, and 14 days after modeling, the paw withdrawal mechanical threshold and paw withdrawal thermal latency were both decreased in the model group compared with the control group, while the levels of phospholipase A2, cyclooxygenase 2, prostaglandin E2, tumor necrosis factor α, interleukin 1β, LC3I and Beclin-1 increased (P < 0.05). The above indexes showed no significant changes in the miR-206 inhibitor-NC group and miR-206 mimics-NC group compared with the model group (P > 0.05). Compared with the miR-206 mimics-NC group, the miR-206 mimics group had lower paw withdrawal mechanical threshold and paw withdrawal thermal latency and higher levels of phospholipase A2, cyclooxygenase 2, prostaglandin E2, tumor necrosis factor α, interleukin 1β, LC3I, and Beclin-1 levels (P < 0.05). Compared with the miR-206 inhibitor-NC group, the rats in the miR-206 inhibitor group showed opposite changes in the above indicators, and there were significant differences between the two groups (P < 0.05). To conclude, inhibition of miR-206 can significantly improve the level of inflammatory factors in nucleus pulposus of rats with lumbar disc herniation, increase pain threshold, and reduce autophagy. The mechanism is related to the inhibition of LC3I and Beclin-1 expression.

Key words: lumbar disc herniation, miR-206, inflammation, analgesia, autophagy