脂多糖对小鼠巨噬细胞ABCA1表达和胆固醇流出的影响.pdf

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1、中南医学科学杂志2014年3月第42卷第2期l39文章编号：2095—1116(2014)02—0139—05·基础医学·脂多糖对小鼠巨噬细胞ABCA1表达和胆固醇流出的影响曾志青。李金凤，谢笛，汤石林(1．南华大学附属第一医院神经外科，湖南衡阳421001；2．南华大学医学院；3．南华大学附属第一医院重症医学科)摘要：目的观察脂多糖(LPS)对小鼠腹腔巨噬细胞ATP结合盒转运体A1(ABCA1)表达和胆固醇流出的影响，探讨肝x受体Ot(LXRa)信号途径的作用。方法60只C57小鼠分成两组，分别注射LPS(1．0mg／kg)和等量生理盐水。1

2、2h后取腹腔巨噬细胞，实时荧光定量PCR和Western—blot印迹法检测ABCA1和LXRamRNA和蛋白质表达水平，液体闪烁计数器检测细胞内胆固醇流出。LXRct激动剂22(R)一羟基胆固醇(22(R)-Hch)预处理小鼠，观察对LPS调节ABCA1表达和胆固醇流出的影响。结果LPS抑制LXRc~和ABCA1的mRNA和蛋白质表达；22(R)一Hch预处理抑制LPS对ABCA1表达和胆固醇流出的下调作用。结论通过抑制TLR4／LXRa信号途径的激活，可以减轻LPS诱导的急性时相反应中的炎症程度，上调ABCA1的表达，促进细胞内胆固醇的流出

3、。关键词：脂多糖；肝x受体0l；炎症；三磷酸腺苷结合盒转运体A1中图分类号：R453．9文献标识码：ATheEfectofLip0p0lysaccharide·InducedAcutePhaseReactiononExpressionofABCA1inMacrophagesofMiceZENGZhiqing，LIJinfeng，XIEDi，etal(DepartmentofNeurosurgery，theFirstAffiliatedHospital，UniversityofSouthChina，Hengyang，Hunan421001，Chi

4、na)Abstract：ObjectiveToinvestigatetheeffectoflipopolysaccharide(LPS)ontheexpressionoftheABCA1andcholesteroleffluxinmacrophagesofmice．thero]eofLxRinthisprocesswasalsoobserved．Methods60C57miceweredividedintotwogroups．TheexperimentalgroupweretreatedwithLPS(1．0mg／kg)．Thecontrolg

5、roupweretreatedwithPBS(1．0mg／kg)．After12h，themRNAandproteinexpressionofABCAIandLXR0【inperitonealmacrophagesofmicewereexaminedbyreversetranscriptase—polymerasechainreaction(RT—PCR)andWestern-blot．Thecholesteroleffluxofmacrophageswasdeterminedbyliquidscintillator．Thecellsweret

6、reatedwithLXRaagonist22(R)一Hch，andtheroleofLXRaintheregulatedeffectofLPSontheexpressionofABCA1wereobserved．ResultsLPSdecreasedtheexpressionofLXRaandABCA1inperitonealmacrophagesofmice．AndtheCholesteroleffluxofmacrophageswasalsoinhibitedbyLPS．Aftertreatedwith22(R)·Heh，theinhib

7、itedeffectofLPSonexpressionofABCA1andcholesteroleffluxwereobvious—lyabolishedinmicemacrophages．LPS—inducedacutephasereactiondown—regulatedtheexpressionofABCA1andde—creasedcellularcholesteroleffluxinmacrophagesofmice，whichmayberelatedtotheLXRc~-dependentpathway．Con-clusionInh

8、ibitingtheactivationofsignalingpathwaysTLR4／LXRc~，whichcanreduceinflammatio