脂多糖对B类I型清道夫受体表达的调节

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-κBp65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-K-κB65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。

Lipopolysaccharide Down-regulates SR-BI Expression in a Nucleus Factor-κB Pathway-dependent Manner

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.