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ID:25097872
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时间:2018-11-18
《咪喹莫特对小鼠哮喘模型气道炎症和stat6表达的影响论文》由会员上传分享,免费在线阅读,更多相关内容在学术论文-天天文库。
1、咪喹莫特对小鼠哮喘模型气道炎症和STAT6表达的影响论文金淑贤,殷凯生,卞涛,陈子庆【关键词】哮喘EffectsofimiquimodonairmationandSTAT6expressioninmousemodelsofasthma【Abstract】AIM:ToobservetheeffectsofaerosolimiquimodontheantigeninducedairmationandtheexpressionsofTh2typechemokinesEotaxin,macrophagederivedchemokine(MDC)a
2、ndthymusandactivationregulatedchemokine(TARC)inmousemodelsofasthma.METHODS:Imiquimodanddexamethasoneinisteredtoimmunizedmicebeforeantigenchallenge.At24hafterthefinalOVAinhalation,theleftsuperiorlungtissuemationberofcellsandclassifythem.Theexpressionsofsignaltransducersand
3、activatorsoftranscription1(STAT1)andsignaltransducersandactivatorsoftranscription6(STAT6)inlungsmunohistochemistryandRNAexpressionsofSTAT1,STAT6,IL4,eotaxinandIFNγinlungsinedbyreversetranscriptasepolymerasechainreaction.RESULTS:①Imiquimodanddexamethasoneattenuatedtheairma
4、tionofasthmaticmice.②Imiquimoddecreasedthetotolcellcounts,EOSandlymphocytecountsinBALf.③TheexpressionsofSTAT1andSTAT6ainlyonthebronchialepithelium.STAT1andSTAT6proteinsandmRNAlevelsincreasedinlungtissuesinasthmagroup.ImiquimodsignificantlyreducedSTAT1andSTAT6proteinandmRN
5、Aexpression.DexamethasonesignificantlyreducedthelevelsofSTAT6proteinandmRNA,butfailedtoinhibittheexpressionofSTAT1.④ImiquimodmodulatedtheTh1/Th2responsebyenhancingTh1cytokineIFNγmRNAandinhibitingtheTh2cytokineIL4mRNAexpressioninlungtissues.CONCLUSION:Imiquimodaerosolinhal
6、ationmayinhibitantigeninducedairmationanddecreasetheoverexpressionofSTAT6proteinandmRNAinasthmaticmousebuthasnoinfluenceonSTAT1expression.【Keya;signaltransducersandactivatoroftranscription1;signaltransducersandactivatoroftranscription6;imiquimod【摘要】目的:观察咪喹莫特对小鼠哮喘模型气道炎症和肺组
7、织信号转导与转录激活因子1(STAT1)和STAT6表达的影响.方法:建立哮喘模型,自14d时雾化吸入OVA前0.5h,干预组分别雾化吸入咪喹莫特30min及ip地塞米松.OVA雾化结束后24h取左上叶肺组织做HE染色观察肺组织炎症改变;收集肺泡灌洗液进行细胞计数和分类;用免疫组化和ann1表达,促进炎性细胞从血管内募集到炎症部位.咪喹莫特是一种免疫调节剂,它由单核细胞、巨噬细胞、B细胞和树突状细胞等抗原递呈细胞识别,通过与这些细胞表面受体如Tollreceptor7(TLR7)结合,诱导产生前炎症细胞因子IFNα,TNFα和IL12,这
8、些局部产生的细胞因子促使Th1反应优势的产生[7].体外实验证实它还能促进培养的T淋巴细胞产生IL12和IFNγ,抑制IL4和IL5[4],使原始Th细胞向Th1细胞分化,提示咪喹莫特可能对治
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