Prooxidant-induced c-Src/nuclear factor kappa B-coupled signalling in sensory ganglia mediates cutaneous hyperalgesia.

摘要: Background Persistent pain resulting from peripheral injury/inflammation is associated with altered sensitivity to cutaneous stimuli, which can manifest as hyperalgesia. The role of oxidant stress in the development, progression and maintenance hyperalgesia still not understood. Furthermore, there appears be a relationship between c-Src kinase pathway oxidative stress. Methods We have used novel prooxidant inflammatory model that involves potassium peroxychromate (PPC), unique produces same reactants activated phagocytes. This was investigate oxidant-activated mediating We compared effects PP2 (a Src family inhibitor) siRNA on behavioural sodium stibogluconate (SSG) non-receptor tyrosine phosphatase AG 1478 receptor inhibitor). Results PP2 attenuated PPC-induced thermal hyperalgesia, while SSG enhanced it. had no effect. decreased levels IL-1β, c-Src/inhibitory kappa B complex formed prostaglandin E2 produced dorsal root ganglia (DRG) ipsilateral inflamed paw, increased these parameters. expression activity DRG paw. Conclusions These results confirm prooxidant-activated plays initiating maintaining by regulating stimulus-response coupling tissue pathway. Our data also suggest oxidant-induced dysregulation c-Src/nuclear factor may contribute our understanding transition acute chronic dysfunctional state seen many human diseases.