LncRNA FTX ameliorates neuropathic pain by targeting miR-320a in a rat model of chronic constriction injury.

Abstract

Long non-coding RNAs (lncRNAs) participate in the process of neuropathic pain (NP). Herein, the goal of this research was to examine the roles of lncRNA five prime to XIST (FTX) in influencing chronic constriction injury (CCI)-induced NP. We have established a rat CCI model to simulate NP in vivo. Reverse transcription-quantitative PCR (RT-qPCR) was used to detect mRNA levels of FTX, microRNA (miR)-320a, and runt-related transcription factor 2 (RUNX2) in the spinal cord. This was followed by subsequent regulation of FTX or miR-320a levels in vivo by intrathecal injection of overexpression FTX or miR-320a mimic lentivirus. The behaviour of rat NP the paw withdrawal threshold (PWT) and paw withdrawal latency (PWL). Enzyme-linked immunosorbent assay (ELISA) was used to assess the secretion of pro-inflammatory and anti-inflammatory factors in the spinal cord tissue. A correlation between FTX and miR-320a, and RUNX2 was validated by luciferase reporter. FTX levels were reduced in CCI rats ( p < 0.05), and miR-320a was a direct target of FTX. Overexpression of FTX typically reduced PWL and PWT as well as neuroinflammation thus alleviating NP ( p < 0.05). However, increasing miR-320a reversed the alleviation of FTX on NP, increased PWL and PWT, and promoted neuroinflammation ( p < 0.05). Additionally, RUNX2, which is a miR-320a target gene, was significantly repressed in CCI rats and its expression was increased by FTX, however, this increase was attenuated by elevated miR-320a ( p < 0.05). In the CCI-induced NP rat model, FTX attenuates NP and neuroinflammation by regulating the miR-320a/RUNX2 axis. This provides a new vision for NP treatment.