SNHG5 knockdown alleviates neuropathic pain induced by chronic constriction injury via sponging miR-142-5p and regulating the expression of CAMK2A

Neuropathic pain (NP) is one of the most intractable diseases. The lack of effective therapeutic measures remains a major problem due to the poor understanding of the cause of NP. The aim of the present study was to investigate the effect of the long non-coding RNA small nucleolar RNA host gene 5 (SNHG5) in NP and the underlying molecular mechanism in order to identify possible therapeutic targets. A chronic constriction injury (CCI) mouse model was used to investigate whether SNHG5 prevents NP and the inflammatory response. Luciferase and RNA pull-down assays were used to detect the binding between SNHG5 and miR-142-5p as well as between miR-142-5p and CAMK2A. Western blot and qPCR were used to detect the RNA and protein expression. The results indicated that SNHG5 significantly inhibited CCI-induced NP. In addition, SNHG5 inhibited the inflammatory response through decreasing the release and the mRNA expression of interleukin (IL)-1β, IL-6, IL-10 and tumor necrosis factor-α. Mechanistically, SNHG5 acted via sponging microRNA-142-5p, thereby upregulating the expression of calcium/calmodulin-dependent protein kinase II α (CAMK2A). Further investigation indicated that CAMK2A knockdown also inhibited CCI-induced NP and inflammation. In summary, the present study demonstrated that SNHG5 silencing could alleviate the neuropathic pain induced by chronic constriction injury via sponging miR-142-5p and regulating the expression of CAMK2A.