大黄素甲醚 L1 通过与 ABCB1 无关的作用逆转 ABCB1 介导的多药耐药，而不依赖于 ABCB1 的下调。

Euphorbia factor L1 reverses ABCB1-mediated multidrug resistance involving interaction with ABCB1 independent of ABCB1 downregualtion.

机构信息

State Key Laboratory of Oncology in South China, Cancer Center, Sun Yat-sen University, Guangzhou 510060, PR China.

出版信息

J Cell Biochem. 2011 Apr;112(4):1076-83. doi: 10.1002/jcb.23021.

Abstract

Euphorbia factor L1 (EFL1) belongs to diterpenoids of genus Euphorbia. In this article, its reversal activity against ABCB1-mediated MDR in KBv200 and MCF-7/adr cells was reported. However, EFL1 did not alter the sensitivity of KB and MCF-7 cells to chemotherapeutic agents. Meanwhile, EFL1 significantly increased accumulation of doxorubicin and rhodamine 123 in KBv200 and MCF-7/adr cells, showing no significant influence on that of KB and MCF-7 cells. Furthermore, EFL1 could enhance the ATP hydrolysis activity of ABCB1 stimulated by verapamil. At the same time, EFL1 inhibited the efflux of ABCB1 in KBv200 and MCF-7/adr cells. In addition, EFL1 did not downregulate expression of ABCB1 in KBv200 and MCF-7/adr cells either in mRNA or protein level.

摘要

Euphorbia factor L1 (EFL1) 属于大戟属二萜类化合物。本文报道了其对 KBv200 和 MCF-7/adr 细胞中 ABCB1 介导的 MDR 的逆转活性。然而，EFL1 并未改变 KB 和 MCF-7 细胞对化疗药物的敏感性。同时，EFL1 显著增加了多柔比星和罗丹明 123 在 KBv200 和 MCF-7/adr 细胞中的积累，对 KB 和 MCF-7 细胞的积累没有显著影响。此外，EFL1 可增强维拉帕米刺激的 ABCB1 的 ATP 水解活性。同时，EFL1 抑制了 KBv200 和 MCF-7/adr 细胞中 ABCB1 的外排。此外，EFL1 既没有在 mRNA 水平也没有在蛋白水平下调 KBv200 和 MCF-7/adr 细胞中 ABCB1 的表达。