中国基层医药
中國基層醫藥
중국기층의약
CHINESE JOURNAL OF PRIMARY MEDICINE AND PHARMACY
2011年
8期
1011-1013
,共3页
曹冬黎%王立金%金韬%陈慧
曹鼕黎%王立金%金韜%陳慧
조동려%왕립금%금도%진혜
B类Ⅰ型清道夫受体%脂多糖%核因子-κB
B類Ⅰ型清道伕受體%脂多糖%覈因子-κB
B류Ⅰ형청도부수체%지다당%핵인자-κB
Scavenger receptor class B type Ⅰ%Lipopolysaccharide%Nucleus factor-κB
目的 观察脂多糖(LPS)对THP-1巨噬细胞源性泡沫细胞B类Ⅰ型清道夫受体(SR-BI)表达和胆固醇流出的影响,并探讨核因子-κB(NF-κB)信号途径在此过程中的作用.方法 THP-1巨噬细胞源性泡沫细胞以LPS单独或NF-κB抑制剂对甲苯磺酰-L-苯丙氨酸氯甲基甲酮(TPCK)预处理后再加入LPS处理.Western blot检测SR-BI及核内NF-κB p65蛋白质的表达,液体闪烁计数器检测细胞内胆固醇流出,高效液相色谱分析细胞内总胆固醇、游离胆固醇和胆固醇酯含量.结果 LPS抑制SR-BI蛋白质的表达,而增加核内NF-κBp65蛋白质的表达,LPS使泡沫细胞细胞内胆固醇流出减少,细胞总胆固醇、游离胆固醇与胆固醇酯增加.TPCK预处理后,LPS的这种作用被部分抑制.结论 NF-κB信号途径介导LPS对SR-BI表达及细胞内胆固醇流出的抑制作用.
目的 觀察脂多糖(LPS)對THP-1巨噬細胞源性泡沫細胞B類Ⅰ型清道伕受體(SR-BI)錶達和膽固醇流齣的影響,併探討覈因子-κB(NF-κB)信號途徑在此過程中的作用.方法 THP-1巨噬細胞源性泡沫細胞以LPS單獨或NF-κB抑製劑對甲苯磺酰-L-苯丙氨痠氯甲基甲酮(TPCK)預處理後再加入LPS處理.Western blot檢測SR-BI及覈內NF-κB p65蛋白質的錶達,液體閃爍計數器檢測細胞內膽固醇流齣,高效液相色譜分析細胞內總膽固醇、遊離膽固醇和膽固醇酯含量.結果 LPS抑製SR-BI蛋白質的錶達,而增加覈內NF-κBp65蛋白質的錶達,LPS使泡沫細胞細胞內膽固醇流齣減少,細胞總膽固醇、遊離膽固醇與膽固醇酯增加.TPCK預處理後,LPS的這種作用被部分抑製.結論 NF-κB信號途徑介導LPS對SR-BI錶達及細胞內膽固醇流齣的抑製作用.
목적 관찰지다당(LPS)대THP-1거서세포원성포말세포B류Ⅰ형청도부수체(SR-BI)표체화담고순류출적영향,병탐토핵인자-κB(NF-κB)신호도경재차과정중적작용.방법 THP-1거서세포원성포말세포이LPS단독혹NF-κB억제제대갑분광선-L-분병안산록갑기갑동(TPCK)예처리후재가입LPS처리.Western blot검측SR-BI급핵내NF-κB p65단백질적표체,액체섬삭계수기검측세포내담고순류출,고효액상색보분석세포내총담고순、유리담고순화담고순지함량.결과 LPS억제SR-BI단백질적표체,이증가핵내NF-κBp65단백질적표체,LPS사포말세포세포내담고순류출감소,세포총담고순、유리담고순여담고순지증가.TPCK예처리후,LPS적저충작용피부분억제.결론 NF-κB신호도경개도LPS대SR-BI표체급세포내담고순류출적억제작용.
Objective To investigate the changes of cholesterol efflux,the scavenger receptor class B type Ⅰ(SR-BI) protein expression in THP-1 maerophage derived foam cells treated with Lippolysaecharide (LPS), and to discover the role of NF-κB pathway in this process.Methods The foam cells were treated with LPS along or treated with N-p-Tosyl-L-phenylalanine chloromethyl ketone(TPCK) for 24 h.The protein levels of SR-BI and intranuclear NF-κB p65 were measured by Western blotting.Cellular lipid accumulation was determined by high performance liquid ehromatograpby analysis.Cholesterol efflux was determined by FJ-2107P type liquid scintillator.Results The expression of SR-BI was decreased after treated with LPS,while the intranuclear NF-κB p65 protein level was increased by LPS.The results also showed that cellular lipid accumulation was increased ,while the cellular cholesterol efflux was decreased in THP-1 maerophage derived foam cells after exposed to LPS for 24 h and these changes can be reversed partly by pretreatment with TPCK.Conclusion LPS could down-regulate the expression of SR-BI, promote the accumulation of lipid and decrease cellular cholesterol efflux in THP-1 maerophage derived foam cells ,which should be related to the TLR4/NF-κB dependent pathway.