中文摘要：

目的：探讨高密度脂蛋白（High-density lipoprotein,HDL）对体外模拟脂肪细胞炎症状态下胆固醇流出的保护作用及其机制。方法：将前脂肪细胞株3T3-L1（3T3-L1）诱导分化成为成熟的脂肪细胞后,作为空白对照组,脂肪细胞以脂多糖（LPS,100 ng/ml）刺激6小时,为LPS组;脂肪细胞经LPS（100 ng/ml）刺激6小时后,分别用不同浓度HDL孵育16小时,为10μg/ml HDL＋LPS组、50μg/ml HDL＋LPS组、100μg/ml HDL＋LPS组。采用液体闪烁计数器检测不同浓度的HDL对LPS刺激的脂肪细胞胆固醇流出的影响,并检测细胞内B族Ⅰ型清道夫受体（SR-BI）信使核糖核酸（mRNA）和蛋白表达水平。结果：LPS组的胆固醇流出率（2.5±0.6）%较空白对照组（4.1±0.4）%减少,3种不同浓度的HDL＋LPS组干预后细胞胆固醇流出率较LPS组增加;LPS组SR-BI mRNA和蛋白表达较空白对照组降低,与LPS组相比较,3种不同浓度的HDL＋LPS组SR-BI mRNA和蛋白表达随HDL浓度的增加而递增,差异均有统计学意义（P〈0.05）。结论：炎症状态下脂肪细胞的胆固醇流出减少,通过上调SR-BI表达能促进炎性脂肪细胞内胆固醇的流出,减少胆固醇在脂肪细胞内的蓄积。该作用可能与其促进脂肪细胞表达SR-BI有关。

英文摘要：

Objective：To investigate the protective role of high-density lipoprotein（HDL）on cholesterol efflux in lipopolysacchride（LPS） stimulated 3T3-L1 adipocytes at inflammatory condition. Methods：3T3-L1 pre-adipocytes were induced to differentiated adipocytes as blank control cells（Control group）.Adipocytes were cultured with LPS 100 ng/ml for 6 hours as LPS cells（LPS group）.LPS cells were cultured with various concentrations of HDL for 16 hours as LPS cells＋10 μg HDL（10 μg HDL group）,LPS cells＋50 μg HDL（50 μg HDL group）,and LPS cells＋100 μg HDL（100 μg HDL group）.Cholesterol efflux rate was measured by pre-labeled 3H-cholesterol HDL in conditioned medium.The intracellular（scavenger receptor BI） mRNA and protein expression were examined respectively. Results：The cholesterol efflux rate in LPS group（2.5±0.6）% was lower than that in Control group（4.1±0.4）%.Three HDL＋LPS groups had increased cholesterol efflux than that in LPS group,P0.05 respectively.In LPS group,the SR-BI mRNA and protein expression was lower than those in Control group.Compared with LPS group,the SR-BI mRNA and protein expression were increased with the elevated of HDL concentrations accordingly,P0.05 respectively. Conclusion：Cholesterol efflux rate decreased in adipocytes at LPS stimulated inflammatory condition.HDL up-regulated SR-BI mRNA and protein expression could promote cholesterol efflux and therefore,reduce the cholesterol accumulation in adipocytes.