Chronic constriction injury (CCI) of the sciatic nerve may induce dorsal root ganglion (DRG) neuronal hyperexcitability and behaviorally expressed hyperalgesia. CCI is a model of neuropathic pain. To investigate the association between the expression of protease activated receptor 2 (PAR2), TMEM16A and neuropathic pain, the expression of PAR2 and TMEM16A proteins in the DRG neurons of rats following CCI of the sciatic nerve was investigated. Following the creation of the CCI model, the thermal withdrawal latency (TWL) was examined by a hot plate test. An immunofluorescence assay and western blot assay were performed to determine the expression of PAR2 and TMEM16A proteins in the ipsilateral L4–6 DRG neurons. The concentration of inositol 1,4,5-triphosphate (IP3) in the L4–6 DRG was determined by ELISA. In the CCI-D7 (7 days after CCI) and CCI-D14 (14 days after CCI) treatment groups, the TWL of rats was significantly shorter than that in the sham operated group (P<0.01; n=12). The expression of PAR2 and TMEM16A proteins in the CCI-D7 and CCI-D14 groups were significantly upregulated compared with the sham operated group (P<0.05; n=12). Additionally, it was revealed that PAR2 and TMEM16A were co-expressed in DRG neurons. It was also observed that IP3 significantly increased in the CCI-D7 and CCI-D14 groups compared with the sham operation group (P<0.05; n=6) as PAR2 and TMEM16A also increased. These findings suggest that the upregulation of PAR2 and TMEM16A in DRG neurons, the co-expression of the two proteins and increasing IP3 are critical to the development of neuropathic pain.

Objective The study aims to systematically evaluate the clinical effect of gabapentin in the treatment of postherpetic neuralgia (PHN). Method Data were retrieved electronically from PubMed, Embase, CNKI, the China Biomedical Database, and the Library of Clinical Database, beginning from the time of inception to April 2017, in order to collect data on randomized controlled trials (RCTs) of gabapentin and placebo in PHN treatment. Results A total of 11 RCTs (2376 people) were retrieved. The gabapentin group reported significantly reduced pain intensity [MD=−0.91, 95% CI −1.32 to −0.51, P<0.00001] compared with the placebo group. Those treated with gabapentin also experienced significantly improved sleep quality [SMD=−0.44, 95% CI −0.66 to −0.23, P<0.0001], but were more likely to experience incidence of adverse events, such as somnolence, dizziness, and peripheral edema. Results of the subgroup analysis showed that the source of heterogeneity may be related to the formulations of the drug. Conclusion Gabapentin can be used to effectively and safely treat PHN.