Beitz J, Corsini A, Granata A, Fumagalli R, Mest H J, Paoletti R
Institut für Pharmakologie und Toxikologie, Martin-Luther-Universität Halle-Wittenberg, GDR.
Biomed Biochim Acta. 1988;47(10-11):S153-6.
The influence of trapidil and some of its derivatives (AR 12456, AR 12463, AR 12465) on the LDL receptor mediated uptake and degradation of 125 I-LDL by human skin fibroblasts (HSF) and human hepatic cells (HEP G2) was investigated. AR 12456 enhanced the uptake and degradation of 125 I-LDL in HEP G2, but inhibited this pathway in HSF. When this drug was preincubated with HEP G2 cells, and then the incubation medium was transferred to HSF, a stimulation of specific LDL pathway occurred also in this cell line. Trapidil, AR 12463 and AR 12465 were inactive under the same experimental conditions. These findings suggest that a metabolite of AR 12456 might be responsible for the enhanced expression of LDL receptors in human cells.
研究了曲匹地尔及其某些衍生物（AR 12456、AR 12463、AR 12465）对人皮肤成纤维细胞（HSF）和人肝细胞（HEP G2）中低密度脂蛋白（LDL）受体介导的125I-LDL摄取和降解的影响。AR 12456增强了HEP G2中125I-LDL的摄取和降解，但在HSF中抑制了该途径。当该药物与HEP G2细胞预孵育，然后将孵育培养基转移至HSF时，该细胞系中特异性LDL途径也受到刺激。在相同实验条件下，曲匹地尔、AR 12463和AR 12465无活性。这些发现表明，AR 12456的一种代谢产物可能是人细胞中LDL受体表达增强的原因。
