ABSTRACT
Aim To investigate the effect of intrathecal injection of fluorocitrate(Fc)on mechanical and thermal hyperalgesia induced by complete Freund's adjuvant(CFA)injection in rats.Methods The mechanical withdrawal threshold(MWT)and thermal withdrawal latency(TWL)were measured before and after CFA or Fc treatment.The changes of glial fibrillary acidic protein(GFAP)and OX-42(a microglial marker)expression in the spinal cord dorsal horn were evaluated by immunohistochemistry analysis.Results Rats with CFA-induced arthritis showed mechanical allodynia and thermal hyperalgesia,which was correlated with the increased GFAP and OX-42 expression in the spinal cord dorsal horn.Intrathecal injection of Fc markedly suppressed CFA-induced thermal hyperalgesia and mechanical allodynia.Fc significantly attenuated the activation of GFAP and OX-42 in the spinal cord dorsal horn.Conclusions The glia activation in spinal cord is closely related to the progress of CFA-induced peripheral hyperalgesia.Fc may exert antihyperalgesic effect by inhibiting the activation of astrocyte and microglia.
ABSTRACT
Objective To observe the activation of astrocytes,microglia and expression of proinflammatory cytokines in the periaqueductal gray(PAG) by Complete Freunds Adjuvant(CFA)-induced inflammatory pain. Methods Heat hyperalgesia and mechanical allodynia were observed and the expressions of mRNA,protein of glial markers,and proinflammatory cytokines in the PAG were examined following intraplantar administration CFA in right hindpaw of the rat by behavioral testing,reverse transcription polymerase chain reaction(RT-PCR), Western blotting,and immunohistochemistry. Results CFA injection induced chronic thermal hyperalgesia and mechanical allodynia.After injection,the thermal hyperalgesia was recovered on Day 14,but the mechanical allodynia lasted more than 21 days.Microglial marker(Cluster of differentiation 14,CD14) and proinflammatory cytokines(Interleukinin-1?,tumor necrosis factor-?) showed a significant increase in their expression during all phases(acute,subacute and chronic) of inflammation.GFAP was observed only in PAG at subacute and chronic phases of inflammation.Conclusion The activation of microglia and astrocytes may be involved in the initiation and maintenance of inflammatory pain.Enhanced cytokines expression might play a role in eliciting behavioral hypersensitivity.