Overexpression of miR-30a attenuates neuropathic pain by targeting SOCS1 in rats with chronic constriction injury

Objectives: To explore the impact of miR-30a on neuropathic pain and associated mechanism. Methods: Sprague-Dawley (SD) rats were randomly assigned to bilateral chronic constriction injury (bCCI) group, sham group, and control group (ten in each group). Expression of miR-30a and suppressors of cytokine signaling (SOCS) 1 were determined by quantitative real time RT-PCR (qRT-PCR). Then another 40 rats were induced model of bCCI and were randomly assigned to overexpression of miR-30a group and its control group, silencing of SOCS1 group and its control group using recombinant lentivirusvectors. The expression of miR-30a and SOCS1 after lentivirus transduction was evaluated by qRT-PCR and Western blotting, respectively. The rats in the four groups were assessed by neurobehavioral tests (mechanical hyperalgesia testing, thermal preference testing (TPT), and acetone testing) before surgery and at days 3, 7, and 14 after surgery. Results: The level of miR-30a was significantly decreased in the bCCI group than that in the sham group and control group, but the level of SOCS1 was significantly increased (P< 0.05). Besides, SOCS1 was a target gene of miR-30a and was negatively regulated by miR-30a. The mechanical shrinkage threshold (MWT) and paw withdrawal thermal latencies (PWTL) were significantly increased, while the frequency was significantly decreased in the overexpression of miR-30a group and knockout of SOCS1 group than those in their corresponding control groups (P< 0.05). Conclusion: Overexpression of miR-30a attenuates neuropathic pain maybe by targeting SOCS1.