An antagonist of the retinoid X receptor reduces the viability of Trichuris muris in vitro.
An antagonist of the retinoid X receptor reduces the viability of Trichuris muris in vitro.
复制标题
类视钉X受体的拮抗剂可在体外降低毛尿症的生存能力。
DOI：
10.1186/1471-2334-14-520
复制
发表时间：
2014-09-27
影响因子：
3.7
通讯作者：
Else KJ
中科院分区：
文献类型：
--
作者：
Hurst RJ;Hopwood T;Gallagher AL;Partridge FA;Burgis T;Sattelle DB;Else KJ
鞭虫病是一种由人类鞭虫 Trichuris trichiura 引起的寄生虫病。它影响着全世界数百万人，特别是在热带地区。这种线虫寄生虫钻入结肠上皮，导致炎症和发病，特别是在儿童中。目前的治疗主要依赖于甲苯咪唑等一般驱虫药，但对这些药物的耐药性日益成为问题。因此，迫切需要新的治疗方法。通过对小鼠鞭虫鞭虫进行多次活力测定，研究了使用视黄醇 X 受体 (RXR) 拮抗剂 HX531 作为新型驱虫药的前景。 HX531 降低了鼠 T. muris 在 L3、L4 和成虫阶段的运动性和活力。此外，生物信息学分析表明，T. muris 基因组拥有 RXR 样受体，这是 HX531 的可能靶标。该研究表明，鞭虫病特异性 RXR 拮抗剂可能是治疗鞭虫病急需的新型驱虫候选药物的来源。 T. muris 基因组中 RXR 样序列的鉴定也为基于这种新的驱虫先导化合物的进一步研究铺平了道路。本文的在线版本 (doi:10.1186/1471-2334-14-520) 包含补充材料，可供授权用户使用。
Trichuriasis is a parasitic disease caused by the human whipworm, Trichuris trichiura. It affects millions worldwide, particularly in the tropics. This nematode parasite burrows into the colonic epithelium resulting in inflammation and morbidity, especially in children. Current treatment relies mainly on general anthelmintics such as mebendazole but resistance to these drugs is increasingly problematic. Therefore, new treatments are urgently required. The prospect of using the retinoid X receptor (RXR) antagonist HX531 as a novel anthelmintic was investigated by carrying out multiple viability assays with the mouse whipworm Trichuris muris. HX531 reduced both the motility and viability of T. muris at its L3, L4 and adult stages. Further, bioinformatic analyses show that the T. muris genome possesses an RXR-like receptor, a possible target for HX531. The study suggested that Trichuris-specific RXR antagonists may be a source of much-needed novel anthelmintic candidates for the treatment of trichuriasis. The identification of an RXR-like sequence in the T. muris genome also paves the way for further research based on this new anthelmintic lead compound. The online version of this article (doi:10.1186/1471-2334-14-520) contains supplementary material, which is available to authorized users.