口服还原型谷胱甘肽联合阿托伐他汀钙对大鼠血脂影响及抗氧化作用-effect of oral reduced glutathione combined with atorvastatin calcium on blood lipid and antioxidation in rats.docx

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口服还原型谷胱甘肽联合阿托伐他汀钙对大鼠血脂影响及抗氧化作用-effect of oral reduced glutathione combined with atorvastatin calcium on blood lipid and antioxidation in rats.docx

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口服还原型谷胱甘肽联合阿托伐他汀钙对大鼠血脂影响及抗氧化作用-effect of oral reduced glutathione combined with atorvastatin calcium on blood lipid and antioxidation in rats

结论1对于高脂血症大鼠模型，还原型谷胱甘肽具有护肝作用外，还具调脂作用，可能与其抗氧化作用有关。2还原型谷胱甘肽与阿托伐他汀钙在调脂及抗氧化作用方面可能潜在协同作用。关键词脂质过氧化还原型谷胱甘肽阿托伐他汀脂肪肝Theimpactofatorvastatin-reducedglutathionecombinationtoanti-oxidationactionandbloodlipidlevelinratswithhyperlipidemiaTutorprof：HeZhaoChuMMED：FangXiangMingTheFirstfirstaffiliatedhospitalofGuangzhoumedicalcollegeAbstractBackgroundsReactiveoxygenspecies(ROS)arepartofoxygenreductionproductsduringoxidativestressinvariouscells.ComponentsofROS[superoxideanion(O-2·),hydrogenperoxide(H2O2),peroxinitriteanions(ONOO-),etc.]areproducedbyvesicularwallendothelialcellsundertheactionsofNADPHoxygenize,hypoxanthineoxidize,lipoidsandendothelialnitricoxidesyntheses(eNOS)duringaerobicrespiration.Meanwhile,excessiveoxidationcanbeprotectedbyenzymaticmechanisms[superoxidedisputes(SOD),catalane(CAT),glutathioneperoxides(GPX),glutathione(GSH),vitaminC(VitC),vitaminE(VitE),etc.])Aswellasnon-enzymaticmechanismsofthebody.Underphysiologicconditions,dynamicequilibriumofROSismaintainedbycontinuousproductionandclearanceofanti-oxidativesystem.Lipidhyperoxidationandirreversiblelesiontocellularmembranes,proteinandDNAarebothresultedfromexcessiveproductionofROSbyvesicularwallendothelialcellsthatsurpassestheprotectioncapacity.Oxidativestresslesiontothevesicularwall,manifestedasendothelialcelldysfunction,structuralabnormality,migrationofmonocytes-macrophages,smoothmusclecellsandfibroblastshyperplasiaandextracellularcomponentdegradation,wouldultimatelyprogresstoatherosclerosis(AS).PeterLibbyetalrevealednosignificantcorrelationbetweenpathogenesisofASandmacrophageuptakeoflowdensitylipoprotein(LDL)prototype,whilesignificantpositivecorrelationwasfoundinuptakeofoxidizedLDL(ox-LDL).TheincreaseinthelevelofROSinducedbyoxidativestresscouldoxidizeLDLintoox-LDL.However,promotionofexcessivemacrophageuptakeoflipidsisthenotthesingleactionthatox-LDLleadstoAS.RecentstudiesrevealedthatAScouldbeinitiatedandpromotedthroughformationoffoamcells,cellularadhesiontoendothelialcellsandchemotaxistosub-endothelium,degradationofm