烟酸对巨噬细胞raw264．7胆固醇流出的影响

Effect of Niacin on Cholesterol Efflux in Macrophage Raw264.7 Cells

【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（raw264．7细胞株）给予不同浓度的烟酸（0～5．0mM）干预24h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（ABCGl），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Westernblot印迹检测ABCGl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ABCGl121RNA及蛋白的表达，并促进其介导的胆固醇流出。LXRa和PPART在巨噬细胞有较高水平的表达，与空白组比较，LXRa，PPART表达在5．0mM浓度的烟酸干预时明显升高。【结论】烟酸可促进巨噬细胞ABCGl介导的胆固醇流出通路，这种作用可能与烟酸上调PPARy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。

[Objective] To observe the effect of niacin on cholesterol efflux in macrophages, and to explore the possible mechanism. [Methods] Macrophage 264.7 ceils 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 reeeptor-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 ABCGl-mediated cholesterol efflux in Raw264, 7 ceils. The expression of LXRa and PPARy in Raw264.7 cells was high. Compared with control group, the expression of LXRa and PPAR）＇ inter- 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 PPAR7 expression. It can provide the clue to explain the mechanisms of high density lipoprotein cholesterol raised by niacin.