姜黄素通过LXRα-ABCA1通路抑制小鼠巨噬细胞脂质聚集  

Curcumin Inhibits Lipid Deposition of Macrophage through LXRα-ABCA1 Pathway in Mouse

作　　者：郑伟[1] 李强[2] 陈欣[1] 李亚新[1] 李珊[1,2] 

机构地区：[1]湖北医药学院附属东风医院综合医疗科,湖北十堰442000 [2]湖北医药学院生物化学教研室,湖北十堰442000

出　　处：《湖北医药学院学报》2015年第2期120-124,F0004,共6页Journal of Hubei University of Medicine

基　　金：湖北省教育厅科学技术研究计划优秀中青年人才基金资助项目(Q20132105);湖北医药学院研究生启动金(2008QDJ18)

摘　　要：目的：探讨姜黄素（curcumine,CUR）对氧化低密度脂蛋白（oxidized low-density lipoprotein,ox-LDL）所致小鼠巨噬细胞泡沫化过程中脂质聚集的影响及其机制。方法：体外培养小鼠巨噬细胞株RAW264.7,分别采用oxLDL（50 mg/L）和Dil（Dioctadecyl）-ox-LDL（10 mg/L）处理细胞24 h,将细胞培养于含不同浓度CUR（0.1~50.0μmol/L）的培养基,MTT法筛选合适的实验浓度;荧光共聚焦显微镜观察Dil-ox-LDL处理后脂质聚集情况;酶学终点法定量细胞内总胆固醇和游离胆固醇的变化;蛋白免疫印迹法检测细胞LXRα和ABCA1的表达水平。结果：与泡沫化组相比,CUR治疗组脂质聚集显著下降;总胆固醇和游离胆固醇的含量均明显下调;另外CUR可以在蛋白水平上引起LXRα和ABCA1的高表达。结论：CUR具有抑制ox-LDL氧化小鼠巨噬细胞脂质聚集的作用,且该作用可能与其上调LXRα-ABCA1表达从而调节细胞内胆固醇的含量有关。Objective To explore the effect and mechanism of curcumin（CUR） on the lipid deposition induced by oxidized low-density hpoprotein（ox-LDL） in the formation of macrophage derived foam ceils in mice. Methods RAW264.7 ceils were respectively treated with ox-LDL （50rag/L） and Dil （Dioctadecyl） -ox-LDL （10rag/L） for 24 h, and then cultured with the medium containing different concentrations（0.1 ~ 50.0 Ixmol/L） of CUR. Cell activity was detected by MTY. Con- focal fluorescence microscopy was used to detect the lipid deposition in the cells. The contents of total cholesterol and free cholesterol were detected by enzymatic endpoint method. The expressions of LXRct and ABCA1 were analyzed by western blotting. Results Compared with foam cell group, the lipid deposition, the contents of total cholesterol and free cholesterol were all significantly decreased in CUR treatment group. Meanwhile, CUR upregulated the protein expressions of LXR（α and ABCA1. Conclusion CUR inhibits ox-LDL-induced lipid deposition in macrophages of mouse, which may correlate with the upregulation of LXRα-ABCA1 expression regulating the content of cellular cholesterol.

关 键 词：姜黄素 巨噬细胞 脂质沉积 LXRΑ ABCA1 

分 类 号：R285.5[医药卫生—中药学]