Ubiquitin‑specific peptidase 53 promotes chronic constriction injury‑induced neuropathic pain through the RhoA/ROCK pathway.

Abstract

Neuropathic pain is associated with nervous system injury and the production of pro‑inflammatory factors. Critical functions for ubiquitin‑specific peptidase 53 (USP53) have been demonstrated in various diseases. However, the role and mechanism of USP53 in chronic constriction injury (CCI)‑induced neuropathic remains unclear. In our current study, a model of neuropathic pain was induced by CCI in rats. Quantitative reverse transcription‑polymerase chain reaction (qRT‑PCR) and western blotting results demonstrated that USP53 was significantly up‑regulated in CCI rats. In addition, silencing of USP53 alleviated neuropathic pain and reduced the production of pro‑inflammatory factors in CCI rats according to paw withdrawal threshold (PWT) and paw withdrawal latency (PWL) tests and enzyme‑linked immunosorbent assay (ELISA), respectively. Moreover, knockdown of USP53 inhibited the activation of FK506‑binding protein 51 (FKBP51)/RhoA/ROCK signaling in CCI rats. In summary, this study revealed that USP53 exacerbated CCI‑induced neuropathic pain, potentially via regulation of the FKBP51/RhoA/ROCK pathway.