Zhou Shufeng, Li Yan, Kestell Phillip, Schafer Peter, Chan Eli, Paxton James W
Department of Pharmacology and Clinical Pharmacology, Faculty of Medical and Health Sciences, the University of Auckland, Auckland, New Zealand.
Eur J Drug Metab Pharmacokinet. 2005 Jan-Jun;30(1-2):49-61. doi: 10.1007/BF03226408.
Studies in patients have indicated that the oral absorption of thalidomide is considerably variable at high doses (>200 mg/day). The aim of this study was to investigate the transport of racemic thalidomide using human colon cancer cell line (Caco-2) monolayers, which have been widely used to investigate drug permeability. A typical 21-day protocol was used to prepare Caco-2 monolayers. Thalidomide was determined by a validated high performance liquid chromatography method with ultraviolet detection. The integrity of Caco-2 monolayer was confirmed when the transepithelial electrical resistance (TEER) exceeded 300 Ohmz . cm2, and the leakage of 14C-manitol was <1% per hour. Uptake of thalidomide by Caco-2 cells was very limited (up to 2.1%). The transport of thalidomide appeared to be linear up to 1 hr. Our study indicated that the permeability coefficients (Papp) of thalidomide at 2.5-300 microM from the apical (AP) to basolateral (BL) and from BL to AP side was 2-6 x 10(-5) cm/sec, with a marked decrease in Papp values from AP to BL at increased thalidomide concentration. The transport of thalidomide was sodium-, temperature- and pH-dependent, as replacement of extracellular sodium chloride or reducing temperature and apical pH can result in significant decreases in the Papp values. Additional data indicated that transport of thalidomide is energy-dependent, as it was significantly (P < 0.05) inhibited by the ATP inhibitors, sodium azide and 2,4-dinitrophenol. In addition, DL-glutamic acid, cytidine, diprodomole, papaverine, quinidine, and cyclophosphamide significantly (P < 0.05) inhibited the transport of thalidomide, while the P-glycoprotein inhibitor verapamil and other nucleosides and nucleotides such as thymidine and guanine had no effect. These results indicated that thalidomide was rapidly transported by Caco-2 monolayers, and this might involve a saturable energy-dependent transporter.
针对患者的研究表明,沙利度胺在高剂量(>200毫克/天)时口服吸收存在显著差异。本研究的目的是利用人结肠癌细胞系(Caco-2)单层细胞来研究外消旋沙利度胺的转运情况,该细胞系已被广泛用于研究药物渗透性。采用典型的21天方案制备Caco-2单层细胞。沙利度胺通过经过验证的带有紫外检测的高效液相色谱法进行测定。当跨上皮电阻(TEER)超过300欧姆·平方厘米且14C-甘露醇的泄漏率每小时<1%时,确认Caco-2单层细胞的完整性。Caco-2细胞对沙利度胺的摄取非常有限(高达2.1%)。沙利度胺的转运在长达1小时内似乎呈线性。我们的研究表明,沙利度胺在2.5 - 300微摩尔浓度下从顶端(AP)到基底外侧(BL)以及从BL到AP侧的渗透系数(Papp)为2 - 6×10(-5)厘米/秒,随着沙利度胺浓度增加,从AP到BL的Papp值显著降低。沙利度胺的转运依赖于钠、温度和pH值,因为替换细胞外氯化钠或降低温度以及顶端pH值会导致Papp值显著降低。额外的数据表明,沙利度胺的转运依赖能量,因为它被ATP抑制剂叠氮化钠和2,4 - 二硝基苯酚显著(P < 0.05)抑制。此外,DL - 谷氨酸、胞苷、双嘧达莫、罂粟碱、奎尼丁和环磷酰胺显著(P < 0.05)抑制沙利度胺的转运,而P - 糖蛋白抑制剂维拉帕米以及其他核苷和核苷酸如胸苷和鸟嘌呤则没有影响。这些结果表明,沙利度胺可被Caco-2单层细胞快速转运,这可能涉及一种可饱和的能量依赖性转运体。