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Inflammatory pain activates astrocytes and increases inflammatory cytokine release in the spinal cord.Mitochondrial fusion and fission rely on the functions of dynamin-related protein 1 (Drp1)and optic atrophy 1 (OPA1),which are essential for the synaptic transmission and plasticity.In the present study,we aimed to explore the effects of 2-bromopalmitate (2-BP),an inhibitor of protein palmitoylation,on the modulation of pain behavior.Rats were intraplantar injected with complete Freund's adjuvant (CFA) to establish an inflammatory pain model.In the spinal cord of rats with CFA-induced inflammatory pain,the expression of astrocyte-specific glial fibrillary acidic protein (GFAP) and contents of proinflammatory cytokines IL-1β and TNF-α were increased.Mito-chondrial Drp1 was increased,while OPA1 was decreased.Consequently,CFA induced reactive oxygen species (ROS) production and Bcl-2-associated X protein (BAX) expression.The intrathe-cal administration of 2-BP significantly reversed the pain behaviors of the inflammatory pain in rats.Moreover,2-BP also reduced the Drp1 expression,elevated the OPA1 expression,and further reduced the GFAP IL-1β,and TNF-α expression and ROS production.Furthermore,in vitro study proved a similar effect of 2-BP on the regulation of Drp1 and OPA1 expression.2-BP also increased the mitochondrial membrane potential and decreased the levels of BAX,ROS,and proinflamma-tory cytokines.These results indicate that 2-BP may attenuate the inflammatory pain of CFA-treated rats via regulating mitochondrial fission/fusion balance and function.