中文摘要：

目的：研究过氧化体增殖物激活型受体-1（peroxisome proliferator activated receptors-γ，PPAR-γ）配体罗格列酮对巨噬细胞酰基辅酶A：胆固醇酰基转移酶-γ（Acyl—CoA：cholesterol acyltransferase-1，ACAT-1）表达的影响及可能机制。方法：在RPMI 1640培养基中培养人单核细胞株（THP-1），加入佛波酯培养48h，细胞贴壁呈巨噬细胞样分化。将细胞分为空白对照组、不同浓度罗格列酮组和罗格列酮＋渥曼青霉素（wortmannin）组，运用实时定量PCR和Western blot，观察巨噬细胞ACAT-1 mRNA和蛋白表达水平的变化。结果：罗格列酮可明显抑制ACAT-1 mRNA和蛋白的表达，且呈浓度依赖性；加入磷酯酰肌醇三磷酸激酶（phosphate dylinositol 3-kinase，PI3K）信号途径抑制剂渥曼青霉素后ACAT-1表达较罗格列酮组高，较空白对照组低。结论：PPAR-1配体罗格列酮通过P13K途径抑制ACAT-1表达发挥其抗动脉粥样硬化的作用。

英文摘要：

Objective To investigate the effect of the peroxisome proliferator activated receptors-γ （PPAR-γ） hgand rosiglitazone on Acyl-CoA：cholesterol acyhransferases-1 （ACAT-1） expression in human macrophages and its possible mechanisms. Methods Human monocytic cell line THP-1 was cultured in the RPMI 1640 media and then incubated with phorbol myristate acetate for 48 hours. Cell adherence demonstrated macrophage-like differentiation. The macrophage-like cells were divided into control group, groups with rosiglitazone at various concentrations, and rosiglitazone/ wortmannin group. The expressions of ACAT-1 mRNA and its proteins in the cells were determined by real-time quantitative polymerase chain reaction and Western blot. Results The expressions of ACAT-1 mRNA and its proteins were obviously inhibited by rosiglitazone in a concentration-dependent fashion, but they were evidently increased following the treatment of phosphate dylinositol 3-kinase （PI3K） inhibitor wortmannin, and still lower than those in the control group. Conclusion Rosiglitazone protects against atherosclerosis by suppressing ACAT-1 expression via PI3K signal transduction pathways.