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雷帕霉素预处理对大鼠肾脏缺血再灌注损伤的保护作用.docx

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雷帕霉素预处理对大鼠肾脏缺血再灌注损伤的保护作用 Abstract Renalischemia-reperfusioninjury(IRI)isacommoneventthatcanresultinacutekidneyinjuryandrenaldysfunction.Recentstudiessuggestthatpretreatmentwithrapamycin,apotentimmunosuppressantandantiproliferativeagent,mayhaveaprotectiveeffectagainstrenalIRI.Inthispaper,wereviewthepathophysiologyofrenalIRI,themechanismsofactionofrapamycin,andtheresultsofrecentstudiesinvestigatingthepotentialprotectiveeffectofrapamycinpretreatmentinratswithrenalIRI. Introduction Renalischemia-reperfusioninjury(IRI)isacommoneventthatoccursduringkidneytransplantation,majorsurgeries,andshockstates.Itischaracterizedbyaseriesofcomplexanddynamicpathophysiologicaleventsthatleadtooxidativestress,inflammation,andrenaldysfunction.Despiteextensiveresearch,thetreatmentofrenalIRIremainsdifficult,andthereiscurrentlynoeffectivepharmacologicalinterventionavailableforclinicaluse. Rapamycin,alsoknownassirolimus,isapotentimmunosuppressantandantiproliferativeagentthathasbeenusedextensivelyinthetreatmentoforgantransplantationandcancer.RecentstudieshavesuggestedthatrapamycinmayalsohaveaprotectiveeffectagainstrenalIRI.ThispaperreviewsthepathophysiologyofrenalIRI,themechanismsofactionofrapamycin,andtheresultsofrecentstudiesinvestigatingthepotentialprotectiveeffectofrapamycinpretreatmentinratswithrenalIRI. PathophysiologyofRenalIRI RenalIRIisacomplexpathophysiologicalprocessinvolvinganumberofinterconnectedcellularandmolecularevents.Briefly,renalIRIisinitiatedbyaperiodofischemia,duringwhichthereisareductionofbloodflowtothekidneyandaresultantdecreaseinoxygenandnutrientdelivery.Thisleadstoacascadeofevents,includinginflammatorycytokinerelease,endothelialdysfunction,andlossofcellularhomeostasis.Uponreperfusion,acomplexseriesofeventsoccursthatcanresultinfurthertissuedamageandexacerbaterenaldysfunction. InflammatorycytokinereleaseisamajorcontributortothepathophysiologyofrenalIRI.Duringischemia,theischemicinjuriesintherenaltissuereleasepro-inflammatorycytokinessuchastumornecrosisfactor-α(TNF-α),inte