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为什么我们应该保持警惕:体外转运体抑制研究中观察到的药物细胞毒性。

Why we should be vigilant: drug cytotoxicity observed with in vitro transporter inhibition studies.

机构信息

Department of Pharmaceutical Sciences, School of Pharmacy, University of Maryland, 20 N. Pine Street, Baltimore, MD 21201, United States.

出版信息

Biochem Pharmacol. 2010 Oct 1;80(7):1087-92. doi: 10.1016/j.bcp.2010.06.012. Epub 2010 Jun 23.

Abstract

From routine in vitro drug-transporter inhibition assays, observed inhibition is typically assumed from direct interaction with the transporter. Other mechanisms that possibly reduce substrate uptake are not frequently fully examined. The objective of this study was to investigate the association of transporter inhibition with drug cytotoxicity. From a pool of drugs that were identified as known ASBT or OCTN2 inhibitors, 21 drugs were selected to screen inhibitory potency of their prototypical substrate and cytotoxicity against three human sodium-dependent solute carrier (SLC) transporters: apical sodium-dependent bile acid transporter (ASBT), organic cation/carnitine transporter (OCTN2), and the excitatory amino acid transporter 4 (EAAT4) in stable cell lines. Twenty drugs showed apparent inhibition in OCTN2-MDCK and ASBT-MDCK. Four dihydropyridine calcium channel blockers were cytotoxic to MDCK cells, and the observed cytotoxicity of three of them accounted for their apparent OCTN2 inhibition, and consequently were classified as non-OCTN2 inhibitors. Meanwhile, since their cytotoxicity only moderately contributed to ASBT inhibition, these three were still considered ASBT inhibitors. Four other drugs showed apparent inhibition in EAAT4-HEK cells, and cytotoxicity of three drugs corresponded with their inhibition of this transporter. Therefore, cytotoxicity significantly affected EAAT4 observations. Results showed the potential of cytotoxicity as a mechanism that can account for apparent in vitro transporter inhibition. Drug cytotoxicity varied in different cell lines, which could increase false positives for pharmacophore development.

摘要

从常规的体外药物转运体抑制试验中,观察到的抑制作用通常假定是与转运体的直接相互作用所致。其他可能降低底物摄取的机制并不经常被充分检查。本研究的目的是研究转运体抑制与药物细胞毒性之间的关系。从一组被确定为已知 ASBT 或 OCTN2 抑制剂的药物中,选择了 21 种药物来筛选其原型底物的抑制效力,并对三种人源钠依赖性溶质载体(SLC)转运体(顶端钠依赖性胆酸转运体(ASBT)、有机阳离子/肉碱转运体(OCTN2)和兴奋性氨基酸转运体 4(EAAT4))在稳定细胞系中的细胞毒性进行筛选。20 种药物在 OCTN2-MDCK 和 ASBT-MDCK 中表现出明显的抑制作用。四种二氢吡啶钙通道阻滞剂对 MDCK 细胞具有细胞毒性,其中三种的观察到的细胞毒性归因于它们对 OCTN2 的明显抑制作用,因此被归类为非 OCTN2 抑制剂。同时,由于它们的细胞毒性仅对 ASBT 抑制有一定贡献,因此这三种药物仍被认为是 ASBT 抑制剂。另外四种药物在 EAAT4-HEK 细胞中表现出明显的抑制作用,其中三种药物的细胞毒性与它们对该转运体的抑制作用相对应。因此,细胞毒性显著影响了对 EAAT4 的观察。结果表明,细胞毒性作为一种可以解释体外转运体抑制的机制的潜力。药物细胞毒性在不同细胞系中存在差异,这可能会增加药理性研究中假阳性的产生。

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