miR-363-5p protects from neuropathic pain in chronic constriction injury (CCI) rat models and regulates Schwann cell injury via negatively modulating SERPING1.

Abstract

OBJECTIVES: Due to the complex and unclear pathogenesis of neuropathic pain, there is a lack of effective therapeutic strategy. miR-363-5p was considered of great potential in mediating the development of neuropathic pain, which has not been confirmed with direct evidence. This study evaluated the role of miR-363-5p in neuropathic pain with animal and cell models, aiming to reveal the potential of miR-363-5p in target therapy of neuropathic pain. METHODS: Chronic constriction injury (CCI) rat models were established as the neuropathic pain model. The expression of miR-363-5p and its target was evaluated by PCR. The painology behaviors were evaluated to assess the function of miR-363-5p. Schwann cells were induced with LPS mimicking cell injury during neuropathic pain. Inflammation and cell growth were estimated by ELISA and CCK8 assays. RESULTS: Significant downregulation of miR-363-5p and upregulation of SERPING1 were observed in CCI rats. miR-363-5p negatively regulated SERPING1 in CCI rats and LPS-induced Schwann cells. Overexpressing miR-363-5p could improve pain threshold and alleviate inflammation in CCI rats. It also a ttenuated LPS-induced inflammation and reduced proliferation in Schwann cells. The overexpression of SERPING1 could reverse the protective effect of miR-363-5p on CCI rats and LPS-induced Schwann cell injury. CONCLUSION: miR-363-5p protected from neuropathic pain via alleviating Schwann cell injury by negatively modulating SERPING1.