CAJ | 학술논문

[目的]观察烟酸对巨噬细胞胆固醇流出的影响并探讨其机制。[方法]对巨噬细胞（raw 264．7细胞株）给予不同浓度的烟酸（0～5．0 mM）干预24 h 后，收集细胞，反转录聚合酶链反应测定巨噬细胞三磷酸腺苷结合盒转运体 G1（ABCG1），肝 X 受体 a（LXRa）和过氧化物酶增殖物激活受体γ（PPARγ）mRNA 表达及 Western blot 印迹检测 ABCG1和 LXRa 蛋白表达，采用液体闪烁计数器检测细胞内胆固醇流出。[结果]烟酸呈剂量依赖性增加巨噬细胞 ABCG1 mRNA 及蛋白的表达，并促进其介导的胆固醇流出。LXRa 和PPARγ在巨噬细胞有较高水平的表达，与空白组比较，LXRa，PPARγ表达在5．0 mM 浓度的烟酸干预时明显升高。[结论]烟酸可促进巨噬细胞 ABCG1介导的胆固醇流出通路，这种作用可能与烟酸上调 PPARγ和LXRa 表达有关。这可为解释烟酸升高高密度脂蛋白胆固醇的机制提供有用的线索。
[목적]관찰연산대거서세포담고순류출적영향병탐토기궤제。[방법]대거서세포（raw 264．7세포주）급여불동농도적연산（0～5．0 mM）간예24 h 후，수집세포，반전록취합매련반응측정거서세포삼린산선감결합합전운체 G1（ABCG1），간 X 수체 a（LXRa）화과양화물매증식물격활수체γ（PPARγ）mRNA 표체급 Western blot 인적검측 ABCG1화 LXRa 단백표체，채용액체섬삭계수기검측세포내담고순류출。[결과]연산정제량의뢰성증가거서세포 ABCG1 mRNA 급단백적표체，병촉진기개도적담고순류출。LXRa 화PPARγ재거서세포유교고수평적표체，여공백조비교，LXRa，PPARγ표체재5．0 mM 농도적연산간예시명현승고。[결론]연산가촉진거서세포 ABCG1개도적담고순류출통로，저충작용가능여연산상조 PPARγ화LXRa 표체유관。저가위해석연산승고고밀도지단백담고순적궤제제공유용적선색。
[Objective]To observe the effect of niacin on cholesterol efflux in macrophages,and to explore the possible mechanism.[Methods]Macrophage 264.7 cells were incubated in the medium containing various concentration of niacin (0~5.0mM)for 24h.Reverse transcription polymerase chain reaction(RT-PCR)was used to determine the expression of adenosine triphosphate-binding cassette transporter G1(ABCG1),liver X-receptor a(LXRa)and peroxisome proliferator-activated receptor-γ(PPARγ),and Western blot was used to detect the protein expression of ABCG1 and LXRa in macrophages.Liquid scintillation counter was used to de-tect cholesterol efflux.[Results]Niacin dose-dependently increased the mRNA and protein expression of AB-CG1 and promoted ABCG1-mediated cholesterol efflux in Raw264.7 cells.The expression of LXRa and PPARγin Raw264.7 cells was high.Compared with control group,the expression of LXRa and PPARγinter-vened by niacin 5.0mM increased obviously.[Conclusion]Niacin can promote cholesterol efflux pathway me-diated by ABCG1,which may be associated with the up-regulation of LXRa and PPARγ expression.It can provide the clue to explain the mechanisms of high density lipoprotein cholesterol raised by niacin.