摘要
目的研究阿托伐他汀对炎症刺激物脂多糖干预后人脐静脉内皮细胞中肝X受体α及其靶基因腺苷三磷酸结合盒转运体A1、固醇调节元件结合蛋白1表达的影响。方法体外培养人脐静脉内皮细胞,进行以下干预实验:对照组加入2μL磷酸盐缓冲液;脂多糖干预组用终浓度为100μg/L脂多糖溶液干预细胞24 h;(2)对照干预组和阿托伐他汀干预组先用二甲基亚砜或不同浓度(0.1、1.0及10.0μmol/L)的阿托伐他汀预干预2 h,然后加入100μg/L脂多糖溶液共同干预22 h。用实时定量聚合酶链反应测定肝X受体α及其靶基因腺苷三磷酸结合盒转运子A1、固醇调节元件结合蛋白1的mRNA表达量。结果与对照组相比,脂多糖干预组肝X受体α及其靶基因mRNA表达明显受到抑制(P<0.05);与对照干预组相比,阿托伐他汀干预组随给药浓度增加肝X受体α及其靶基因mRNA表达逐步升高(P<0.05)。结论脂多糖可明显抑制人脐静脉内皮细胞中肝X受体α及其靶基因表达;阿托伐他汀在一定范围内可呈剂量依赖性上调肝X受体α及其靶基因表达,提示其抗动脉粥样硬化作用可能部分通过肝X受体信号通路发挥作用。
Aim To investigate the effect of atorvastatin on mRNA expression of liver X receptor α （LXRα） and its target gene ATP-binding cassette transporter A1 （ABCA1）, sterol regulatory element binding protein-1 （ SREBP-1 ） in human umbilical vein endothelial cells （HUVEC） after treated by lipopolysacharide（LPS）. Methods Human umbili- cal vein endothelial cells were cultured in vitro with gibco 1640 medium and 10 percent fetal bovine serum and 1 percent double antibiotics, and then were plated in 6-well plates at a denisity of approximately 2× 10^5 cells per milliliter of media to be intervened. （ 1 ） Control group ： HUVEC were cultured with the completed medium involving phosphate buffered saline （PBS）, and LPS treated group or control intervention group： HUVEC were treated with LPS （the terminal concentration was 100 μg/L） for 24 hours; （2）Atorvastatin intervention group or control intervention group：HUVEC were first treated with atorvastatin at different concentrations （0. 1, 1.0, 10. 0 μmoL/L） or dimethyl sulfoxide （DMSO） for 2 hours, and then co-treated with LPS for 22 hours. The level of LXRα and its target genes mRNA expression were measured by real- time polymerase chain reaction. Results Compared with control group, LPS could inhibit the mRNA expression of LXRα and its target genes ABCA1, SREBP-1 in HUVEC. The differences were statistically significant （ P 〈 0.05）. Compared with LPS plus DMSO group, atorvastatin could upregulate the mRNA expression of LXRα and its target gene mR- NA expression in a dose-dependent manner. The differences were statistically significant （ P 〈 0. 05 ）. Meanwhile, ator- vastatin could downregulate the mRNA expression of inflammatory factor and adhesion factors in a dose-dependent manner.Conclusion These results demonstrate that LPS may inhibit the mRNA expression of LXRα and its target genes in HU- VEC, and atorvastatin can upregulate the mRNA expression of LXRα and its target gene mRNA expression in a dose-de- pendent manner to inhibit the inflammatory state of HUVEC.
出处
《中国动脉硬化杂志》
CAS
CSCD
北大核心
2012年第8期705-708,共4页
Chinese Journal of Arteriosclerosis
关键词
阿托伐他汀
人脐静脉内皮细胞
肝X受体Α
Atorvastatin
Human Umbilical Vein Endothelial Cells
Liver X Receptor α
