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一种与细胞穿透性Tat(48 - 60)肽相连的嵌入BODIPY的米替福新类似物,有利于抗寄生虫药物的细胞内递送和可视化。

A BODIPY-embedding miltefosine analog linked to cell-penetrating Tat(48-60) peptide favors intracellular delivery and visualization of the antiparasitic drug.

作者信息

de la Torre Beatriz G, Hornillos Valentín, Luque-Ortega Juan R, Abengózar M A, Amat-Guerri Francisco, Acuña A Ulises, Rivas Luis, Andreu David

机构信息

Department of Experimental and Health Sciences, Pompeu Fabra University, Barcelona Biomedical Research Park, 08003, Barcelona, Spain.

出版信息

Amino Acids. 2014 Apr;46(4):1047-58. doi: 10.1007/s00726-013-1661-3. Epub 2014 Jan 21.

Abstract

Therapeutic application of many drugs is often hampered by poor or denied access to intracellular targets. A case in point is miltefosine (MT), an orally active antiparasitic drug, which becomes ineffective when parasites develop dysfunctional uptake systems. We report here the synthesis of a fluorescent BODIPY-embedding MT analogue with appropriate thiol functionalization allowing linkage to the cell-penetrating Tat(48-60) peptide through disulfide or thioether linkages. The resulting constructs are efficiently internalized into the otherwise MT-invulnerable R40 Leishmania strain, resulting in fast parasite killing, and hence successful avoidance of the resistance. In the disulfide-linked conjugate, an additional fluoro tag on the Tat moiety allows to monitor its reductive cleavage within the cytoplasm. Terminally differentiated cells such as peritoneal macrophages, impervious to MT unless infected by Leishmania, can uptake the drug in its Tat-conjugated form. The results afford proof-of-principle for using CPP vectors to avert drug resistance in parasites, and/or for tackling leishmaniasis by modulating macrophage uptake.

摘要

许多药物的治疗应用常常因难以或无法作用于细胞内靶点而受到阻碍。一个典型的例子是米替福新(MT),一种口服有效的抗寄生虫药物,当寄生虫的摄取系统出现功能障碍时,它就会失效。我们在此报告一种嵌入荧光BODIPY的MT类似物的合成,该类似物具有适当的硫醇功能化,可通过二硫键或硫醚键与细胞穿透肽Tat(48 - 60)连接。所得构建体能够有效地内化到原本对MT有抗性的R40利什曼原虫菌株中,从而快速杀死寄生虫,成功避免耐药性。在二硫键连接的共轭物中,Tat部分上的额外氟标签可用于监测其在细胞质内的还原裂解。终末分化细胞,如腹膜巨噬细胞,除非被利什曼原虫感染,否则对MT不敏感,但可以摄取其Tat共轭形式的药物。这些结果为使用细胞穿透肽载体来避免寄生虫的耐药性和/或通过调节巨噬细胞摄取来治疗利什曼病提供了原理证明。

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