AnalgesicEffectofElectroacupunctureonPaclitaxel-InducedNeuropathicPainviaSpinalOpioidergicandAdrenergicMechanismsinMice
电针对紫杉醇诱导神经痛的镇痛效果及机制研究
Thisstudywasdesignedtodeterminetheantinociceptiveeffectandrelatedneuronalmechanismofelectroacupuncture(EA)onpaclitaxel(PTX)-inducedneuropathicpaininmice.PTX(4mg/kg,i.p.)wasadministeredonceadayfor5consecutivedaystoinduceneuropathicpain.EAstimulation(2mA,2Hz,30min)wasappliedattheST36acupointbilaterallyonceinevery2days.RepeatedEAstimulationsignificantlyattenuatedPTX-inducedmechanicalallodyniaandthermalhyperalgesia.Inaseparatesetofexperiment,theantinociceptiveeffectofasingleEAstimulation8daysafterPTXtreatmentwasreducedbyintrathecalpretreatmentwithnaloxone(opioidreceptorantagonist),idazoxan(alpha2-adrenoceptorantagonist)orpropranolol(beta-adrenoceptorantagonist),butnotprazosin(alpha1-adrenoceptorantagonist).Moreover,EAremarkablysuppressedthePTX-enhancedphosphorylationoftheNMDAreceptorNR2Bsubunitinthespinaldorsalhorn,andintrathecalpretreatmentofnaloxone,idazoxan(IDA)orpropranololblockedtheeffectofEA.Inconclusion,EAstimulationattheST36acupointsignificantlydiminishedPTX-inducedneuropathicpaininmiceviathemediationofspinalopioidreceptor,alpha2-andbeta-adrenoceptors.
Keywords:Electroacupuncture;ST36;NeuropathicPain;Chemotherapy;Paclitaxel
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