Abstract
BackgroundComplex regional pain syndrome (CRPS) is related to microcirculation impairment caused by tissue hypoxia and peripheral cytokine overproduction in the affected human limb and chronic post-ischemic pain (CPIP) is considered as an animal model for this intractable disease. Previous studies suggest that the pathogenesis of CPIP involves the hypoxia inducible factor-1α (HIF-1α) and an exaggerated regional inflammatory and free radical response. The inhibition of HIF-1α is known to relieve CPIP. So, propofol, as a free radical scavenger, is very likely to be beneficial in terms of relieving CPIP.MethodsWe set up a CPIP model using the hindpaw of mice. We administered propofol (10 mg/kg) just after the reperfusion period (early stage) and also on the second day (late stage), as treatment. The analysis evaluated the expression of HIF-1α, free radicals, and inflammasome.ResultsPropofol administration produced obvious analgesia in both mechanical and thermal evaluation in the early stage of CPIP (2 h after reperfusion). Only a mild analgesic effect was found in the late stage (48 h later after reperfusion). In the early stage, the expression of HIF-1α and the inflammasome marker (NALP1) along with caspase-1 were suppressed by propofol. The free radical level also decreased in the propofol group. But those molecular changes were not founded in the late stage of CPIP.ConclusionOur data demonstrated that propofol produces mice analgesia in the early stage of CPIP and this effect is associated with inhibition of free radical, hypoxia inducible factor and inflammasome.
Highlights
Complex regional pain syndrome (CRPS) is related to microcirculation impairment caused by tissue hypoxia and peripheral cytokine overproduction in the affected human limb and chronic post-ischemic pain (CPIP) is considered as an animal model for this intractable disease
Our results demonstrated that propofol, an reactive oxygen species (ROS) scavenger, can reduce the symptoms of CPIP with its inhibition of hypoxia inducible factor-1α (HIF-1α), inflammasome, and cytokine
We demonstrated that the inflammasome response diminished, and showed that propofol can suppress ROS production, decrease hypoxia-inducible factors (HIFs)-1α, and suppress NALP1 inflammasome along with caspase-1 (Figs. 3 and 4)
Summary
Complex regional pain syndrome (CRPS) is related to microcirculation impairment caused by tissue hypoxia and peripheral cytokine overproduction in the affected human limb and chronic post-ischemic pain (CPIP) is considered as an animal model for this intractable disease. Previous studies suggest that the pathogenesis of CPIP involves the hypoxia inducible factor-1α (HIF-1α) and an exaggerated regional inflammatory and free radical response. Propofol, as a free radical scavenger, is very likely to be beneficial in terms of relieving CPIP. Chronic post-ischemic pain (CPIP)---caused by reperfusion injury---is due to vasoconstriction, tissue hypoxia, and generated cytokines in an affected limb. Previous studies suggested that CPIP includes exaggerated regional inflammatory and hypoxia responses to reperfusion injury [6]. Hypoxia-inducible factors (HIFs)---the transcription factors that respond to oxygen changes---have evidence to fortify the complex regional. The exogenous administration of antioxidant drugs during a reperfusion phase may theoretically attenuate inflammasome and cytokine production in IR injury
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