Institute of Pharmacological Sciences, University of Milan, Via Balzaretti 9, 20133, Milan, Italy.
Cytotechnology. 1993 Jan;11(Suppl 1):S15-7. doi: 10.1007/BF00746043.
The effect of trapidil derivative AR12456 on intracellular cholesterol metabolism was investigated in human hepatoma cell line HepG2. AR12456 enhanced the uptake and degradation of(125)I-LDL in a dose-dependent manner. The drug inhibited cholesterol synthesis and esterification without affecting cellular cholesterol content and bile acid synthesis; cholesterol efflux was slightly increased. These results show that the inhibition of cholesterol synthesis together with the enhanced expression of LDL receptors may partially explain the hypocholesterolemic activity of compound AR12456.
我们研究了曲匹地尔衍生物 AR12456 对人肝癌细胞系 HepG2 细胞内胆固醇代谢的影响。AR12456 呈剂量依赖性地增强(125)I-LDL 的摄取和降解。该药物抑制胆固醇合成和酯化，而不影响细胞内胆固醇含量和胆汁酸合成；胆固醇流出略有增加。这些结果表明，胆固醇合成的抑制与 LDL 受体的表达增强可能部分解释了化合物 AR12456 的降胆固醇活性。
