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1、LeptinAttenuatesLipopolysaccharideorOleicAcid-InducedAcuteLungInjuryinMiceHai-YingDong1,2*,MinXu1,2*,Zhen-YuJi3*,Yan-XiaWang1,2*,Ming-QingDong1,2,Man-LingLiu1,2,Dun-QuanXu1,Peng-TaoZhao1,2,YiLiu1,2,YingLuo1,2,WenNiu1,2,BoZhang1,2,JingYe1,2,andZhi-ChaoLi1,2123Departmentof
2、Pathology,XijingHospital,DepartmentofPathologyandPathophysiology,andDepartmentofMedicalElectronicEngineering,FourthMilitaryMedicalUniversity,Xian,PRChinaLeptinisreportedtobeinvolvedinacutelunginjury(ALI).However,receptor-deficientdb/dbmicehasrecentlybeendemonstrated(9).th
3、eroleandunderlyingmechanismsofleptininALIremainunclear.Incomparisonwithdb/dbmice,leptin-deficientob/obmicepre-TheaimofthisstudywastodeterminewhetherleptindeficiencysentedmarkedimmunesuppressionagainstbacterialpathogenspromotedthedevelopmentofALI.LPSoroleicacid(OA)were(1012
4、)andexhibitedenhancedlethalityandreducedpulmonaryadministeredtowild-typeandleptindeficient(ob/ob)micetoin-bacterialclearance(13).Exogenousleptinadministrationtoob/obduceALI.Leptinlevel,survivalrate,andlunginjurywereexamined.miceimprovedsurvivalandgreatlyimprovedpulmonaryb
5、acterialResultsshowedthatleptinlevelswerepredominantlyincreasedclearance.Despitethesereports,associationbetweenleptinandinthelung,butalsointheheart,liver,kidney,andadiposetissueoutcomesfromALIareinconclusive.afterLPSadminiatration.Comparedwithwild-typemice,LPS-orInthepre
6、sentstudy,wethereforehypothesizedthatleptinde-OA-inducedlunginjurywasworseandthesurvivalratewaslowerficiencymightpromotethedevelopmentofALIandthatahighinob/obmice.Moreover,leptindeficiencypromotedthereleaseoflevelofleptinprotectsagainsttheALIinmice.Theresultsshowedproinflam
7、matorycytokines.Exogenousadministrationofleptinre-thatleptinlevelsinthelungswereincreasedinLPS-inducedALIducedlethalityinob/obmiceandamelioratedlunginjurypartlyinwild-type(WT)mice.Inob/obmice,wealsofoundthatleptinthroughinhibitingtheactivationofNF-kB,p38,andERKpathways.T
8、heseresultsindicatedthatleptindeficiencycontributedtothede-deficiencyreducedsurvivalandenhancedLPS-orolei
