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1、第3期孙亚赛,等:芹菜素通过NF-κB和MAPK抑制脂多糖诱导的骨髓来源的巨噬细胞炎性7芹菜素通过NF-κB和MAPK抑制脂多糖诱导的骨髓来源的巨噬细胞炎性孙亚赛1,贺云1,刘健2,屈玮2*(1.合肥工业大学食品科学与工程学院,合肥230009;2.合肥工业大学生物与医学工程学院,合肥230009)摘要:目的研究芹菜素在脂多糖(lipopolysaccharide,LPS)诱导的骨髓来源的巨噬细胞(bone-marrow-derivedmacrophages,BMDMs)炎性的作用。方法用MTT方法筛选出芹菜素起作用的浓度范围。选择适当的芹菜素浓度处理BMDMs,用实时定量PCR方法检测
2、炎性基因的表达,用Western-blot方法检测炎性信号通路蛋白的表达,以及荧光免疫检验法考察NF-κBP65蛋白的核转位。结果芹菜素的有效作用浓度范围为0~30μmol/L,选用10,30μmol/L浓度的芹菜素培养BMDMs后,炎性因子的mRNA水平明显降低,巨噬细胞从促炎性M1型向抗炎性M2型转化,并且呈现剂量依赖的趋势。NF-κB和MAPK信号通路的激活也受到了明显的抑制。结论芹菜素能通过抑制NF-κB和MAPK信号通路降低LPS诱导的BMDMs的炎性。关键词:芹菜素;骨髓来源的巨噬细胞;脂多糖;NF-κB;MAPKInhibitionofapigeninonlipopolys
3、accharide-inducedbone-marrow-derivedmacrophagesinflammationthroughNF-κBandMAPKSUNYa-Sai1,HEYun1,LIUJian2,QUWei2*(1.SchoolofFoodScienceandEngineering,HefeiUniversityofTechnology,Hefei230009,China;2.SchoolofBiologicalandMedicalEngineering,HefeiUniversityofTechnology,Hefei230009,China)ABSTRACT:Objec
4、tiveToinvestigatetheeffectofapigeninonlipopolysaccharide(LPS)inducedinflammationandinbone-marrow-derivedmacrophages(BMDMs).MethodsTheapigenindosagerangethatdidnotinfluencecellviabilitywasdetectedbyMTTassay.Afterchoosingthesuitabledoseofapigenintoco-culturewithBMDMs,theinflammatorygenesexpressionw
5、asdetectedbyRT-PCR,proteinsexpressionwhichparticipatedininflammatorysignalingpathwayswasdetectedbyWestern-blot,andNF-κBP65nucleartranslocationwasinvestigatedbyimmunofluorescence.ResultsTheeffectivedoseofapigeninwasbetween0~30μmol/L.Bychoosing10and30μmol/Lapigenintoco-culturewithBMDMs,inflammatory
6、cytokineswerereducedinmRNAlevel,BMDMstransformedfromM1inflammatorymacrophagestoanti-inflammatoryM2macrophagesandalltheseresultsshowedinadose-dependentmanner.ApigeninalsoinhibitedNF-κBandMAPKsignalingpathwayssignificantly.第3期孙亚赛,等:芹菜素通过NF-κB和MAPK抑制脂多糖诱导的骨髓来源的巨噬细胞炎性7ConclusionApigenincanreduceLPS-i
7、nducedmacrophagesinflammationandpartlythroughNF-κBandMAPKsignalingpathways.KEYWORDS:apigenin;bone-marrow-derivedmacrophages;lipopolysaccharide;NF-κB;MAPK第3期孙亚赛,等:芹菜素通过NF-κB和MAPK抑制脂多糖诱导的骨髓来源的巨噬细胞炎性71引言炎症被认为是慢性病发病机制的主要因素