医学临床研究
醫學臨床研究
의학림상연구
JOURNAL OF CLINICAL RESEARCH
2013年
9期
1677-1680,1684
,共5页
巨噬细胞%胆固醇%尼克酸
巨噬細胞%膽固醇%尼剋痠
거서세포%담고순%니극산
Macrophages%Cholesterol%Niacin
[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。
[目的]觀察煙痠對巨噬細胞膽固醇流齣的影響併探討其機製。[方法]對巨噬細胞(raw 264.7細胞株)給予不同濃度的煙痠(0~5.0 mM)榦預24 h 後,收集細胞,反轉錄聚閤酶鏈反應測定巨噬細胞三燐痠腺苷結閤盒轉運體 G1(ABCG1),肝 X 受體 a(LXRa)和過氧化物酶增殖物激活受體γ(PPARγ)mRNA 錶達及 Western blot 印跡檢測 ABCG1和 LXRa 蛋白錶達,採用液體閃爍計數器檢測細胞內膽固醇流齣。[結果]煙痠呈劑量依賴性增加巨噬細胞 ABCG1 mRNA 及蛋白的錶達,併促進其介導的膽固醇流齣。LXRa 和PPARγ在巨噬細胞有較高水平的錶達,與空白組比較,LXRa,PPARγ錶達在5.0 mM 濃度的煙痠榦預時明顯升高。[結論]煙痠可促進巨噬細胞 ABCG1介導的膽固醇流齣通路,這種作用可能與煙痠上調 PPARγ和LXRa 錶達有關。這可為解釋煙痠升高高密度脂蛋白膽固醇的機製提供有用的線索。
[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.