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化疗诱导的粘膜炎的暗褐鼠模型:建立与当前技术水平

Dark Agouti rat model of chemotherapy-induced mucositis: establishment and current state of the art.

作者信息

Vanhoecke Barbara, Bateman Emma, Mayo Bronwen, Vanlancker Eline, Stringer Andrea, Thorpe Daniel, Keefe Dorothy

机构信息

Mucositis Research Group, Centre for Personalised Cancer Medicine (CPCM), Centre for Clinical Research Excellence (CCRE) in Oral Health, Faculty of Health Sciences, University of Adelaide, Adelaide, 5005 South Australia, Australia Laboratory of Microbial Ecology and Technology, University of Ghent, 9000 Ghent, Belgium.

Mucositis Research Group, Centre for Personalised Cancer Medicine (CPCM), Centre for Clinical Research Excellence (CCRE) in Oral Health, Faculty of Health Sciences, University of Adelaide, Adelaide, 5005 South Australia, Australia.

出版信息

Exp Biol Med (Maywood). 2015 Jun;240(6):725-41. doi: 10.1177/1535370215581309. Epub 2015 May 12.

DOI:10.1177/1535370215581309
PMID:25966981
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4935219/
Abstract

Mucositis is a major oncological problem. The entire gastrointestinal and genitourinary tract and also other mucosal surfaces can be affected in recipients of radiotherapy, and/or chemotherapy. Major progress has been made in recent years in understanding the mechanisms of oral and small intestinal mucositis, which appears to be more prominent than colonic damage. This progress is largely due to the development of representative laboratory animal models of mucositis. This review focuses on the development and establishment of the Dark Agouti rat mammary adenocarcinoma model by the Mucositis Research Group of the University of Adelaide over the past 20 years to characterize the mechanisms underlying methotrexate-, 5-fluorouracil-, and irinotecan-induced mucositis. It also aims to summarize the results from studies using different animal model systems to identify new molecular and cellular markers of mucositis.

摘要

黏膜炎是一个主要的肿瘤学问题。在接受放疗和/或化疗的患者中,整个胃肠道、泌尿生殖道以及其他黏膜表面都可能受到影响。近年来,在理解口腔和小肠黏膜炎的机制方面取得了重大进展,口腔和小肠黏膜炎似乎比结肠损伤更为突出。这一进展很大程度上归功于具有代表性的黏膜炎实验动物模型的开发。本综述重点介绍了阿德莱德大学黏膜炎研究小组在过去20年中建立的黑褐大鼠乳腺腺癌模型,以阐明甲氨蝶呤、5-氟尿嘧啶和伊立替康诱导黏膜炎的潜在机制。它还旨在总结使用不同动物模型系统的研究结果,以确定黏膜炎新的分子和细胞标志物。

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本文引用的文献

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Development of the rat model of lapatinib-induced diarrhoea.拉帕替尼诱导的大鼠腹泻模型的建立。
Scientifica (Cairo). 2014;2014:194185. doi: 10.1155/2014/194185. Epub 2014 Jul 7.
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Disruption of ZO-1/claudin-4 interaction in relation to inflammatory responses in methotrexate-induced intestinal mucositis.ZO-1/紧密连接蛋白-4 相互作用的破坏与甲氨蝶呤诱导的肠黏膜炎炎症反应有关。
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5-Fluorouracil induced intestinal mucositis via nuclear factor-κB activation by transcriptomic analysis and in vivo bioluminescence imaging.转录组分析和体内生物发光成像显示,5-氟尿嘧啶通过核因子-κB 激活诱导肠道黏膜炎。
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Disruption of the murine Glp2r impairs Paneth cell function and increases susceptibility to small bowel enteritis.破坏小鼠的 Glp2r 会损害潘氏细胞的功能,并增加小肠肠炎的易感性。
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Role of inducible nitric oxide synthase pathway on methotrexate-induced intestinal mucositis in rodents.诱导型一氧化氮合酶通路在鼠类甲氨蝶呤诱导的肠道黏膜炎中的作用。
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Irinotecan injures tight junction and causes bacterial translocation in rat.伊立替康损伤紧密连接并导致大鼠细菌易位。
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Role of platelet-activating factor in the pathogenesis of 5-fluorouracil-induced intestinal mucositis in mice.血小板激活因子在氟尿嘧啶诱导的小鼠肠道黏膜炎发病机制中的作用。
Cancer Chemother Pharmacol. 2011 Sep;68(3):713-20. doi: 10.1007/s00280-010-1540-5. Epub 2010 Dec 14.