| Background:Pulsed radiofrequency(PRF)is a commonly used method for the treatment of zoster-related pain in the clinic.However,PRF therapy has a high recurrence rate and many adverse reactions.Recent studies have shown that short-term spinal cord stimulation(stSCS)can effectively alleviate zoster-related pain.Due to the lack of evidence,it is unclear whether stSCS is superior to PRF in the efficacy of treating zoster-related pain.Objective:This study aimed to compare the efficacy and safety of stSCS and PRF for zoster-related pain.Methods:We searched seven electronic databases from the establishment of the database to January 2021.Related randomized controlled trials were included in this meta-analysis.After extracting the data and evaluating the methodological quality of the included trials,the outcome indicators were statistically analyzed by using RevManV.5.3.Results:This meta-analysis included 6 trials with a total of 509 patients.Compared with PRF group,stSCS group showed lower pain intensity[SMD=-0.83,95%CI(-1.37,-0.30),P=0.002],better sleep quality[MD=-1.43,95%CI(-2.29,-0.57),P=0.001],lower pain rating index scores,and less incidence of adverse events[RR=0.32,95%CI(0.12,0.83),P<0.05].However,the efficacies of PRF and stSCS for treating zoster-related pain were consistent in the response rate[RR=1.10,95%CI(0.82,1.48),P=0.51]and the complete remission rate[RR=1.05,95%CI(0.66,1.68),P=0.84].Conclusions:In this study,stSCS showed a better analgesic effect and higher safety than PRF.Our meta-analysis results suggested that stSCS may be a feasible and safe invasive treatment for zoster-related pain.However,randomized controlled trials with high-quality are needed to further verify our conclusions.Background:Neuropathic pain is a common complication after spinal cord injury(SCI).Because of the poor effects of conventional therapy,neuropathic pain after SCI often brings heavy burden to patients’ body and mind.Therefore,it is vital to explore the mechanisms of neuropathic pain after SCI to develop effective treatment programs or drugs.The current research suggests that neuroinflammation plays a vital role in the generation and maintenance of neuropathic pain after SCI.Receptor-interacting protein kinase 3(RIPK3)is a threonine/serine protein kinase that plays a key role in the inflammatory process.RIPK3 has been shown to promote necroptosis.In addition,some evidence suggested that activated RIPK3 may contribute to inflammation by exerting its non-necroptotic functions,such as activating nuclear factor-κB(NF-κB)or nod-like receptor family pyrin domain-containing protein 3(NLRP3)inflammasome.Previous studies showed that RIPK3 might be involved in inflammatory bowel disease and autoinflammatory disease.However,the role of RIPK3 in neuropathic pain after SCI is unclear.Objective:In this study,to explore the role of RIPK3 in neuropathic pain after SCI,we investigated the expression of RIPK3 in the lumbar spinal cord(L4-6)after thoracic SCI.Meanwhile,we studied the effect of RIPK3 inhibitor on pain behavior,nuclear factor-κB(NF-κB),nod-like receptor family pyrin domain-containing protein 3(NLRP3)inflammasome,and proinflammatory factor.These results may highlight that RIPK3 is a potential target for treating neuropathic pain after SCI.Methods:Thoracic(T10)SCI rat model was conducted,and the mechanical threshold in rats was measured.The expressions of RIPK3,NLRP3,caspase-1,and NF-κB p65 were measured with western blot or quantitative real-time polymerase chain reaction(qRT-PCR).The cell localization of NLRP3 was detected by immunofluorescence staining.In addition,enzyme-linked immunosorbent assay(ELISA)was applied to analyze the levels of proinflammatory factors interleukin 1 beta(IL-1β),interleukin 18(IL-18),and tumor necrosis factor alpha(TNF-α)Results:The expression of RIPK3 increased from postoperative days 7 to postoperative days 21,which was consistent with the development of mechanical allodynia.Intrathecal administration of RIPK3 inhibitor GSK872 could alleviate the mechanical allodynia in SCI rats and reduce the expression levels of RIPK3.The activation of NLRP3 inflammasome and NF-κB p65 were attenuated by GSK872 treatment.Immunofluorescence furthermore suggested that NLRP3 had colocalization with glial cells and neurons in the L4-6 spinal dorsal horns.In addition,GSK872 treatment reduced the production of inflammatory cytokines.Conclusions:Our findings indicated that RIPK3 was an important facilitated factor for SCI-induced mechanical allodynia.RIPK3 inhibition might relieve mechanical allodynia by inhibiting NLRP3 inflammasome,NF-κB,and the associated inflammation. |
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