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使用SKH1小鼠的腺嘌呤诱导慢性肾病简化模型

A Simplified Model of Adenine-Induced Chronic Kidney Disease Using SKH1 Mice.

作者信息

French Benjamin W, Breidenbach Joshua D, Yassine Shereen G, Khatib-Shahidi Bella Z, Kazmi Sara, Murphy Caitlin M, Bashir Humza S, Benson Evan M, Timalsina Bivek, Shrestha Upasana, Faleel Dhilhani, Boyapalli Satkeerth, Dube Prabhatchandra, Lad Apurva, Syed Irum, Malhotra Deepak, Gohara Amira, Kennedy David J, Haller Steven T

机构信息

Department of Medicine, College of Medicine and Life Sciences, University of Toledo, Toledo, OH 43614, USA.

Biochemistry and Biotechnology Group, Bioscience Division, Los Alamos National Laboratory, Los Alamos, NM 87545, USA.

出版信息

Cells. 2024 Dec 20;13(24):2117. doi: 10.3390/cells13242117.

Abstract

Commonly used adenine-induced chronic kidney disease (CKD) murine models often employ C57BL/6 mice; however, this strain has inherent limitations due to its natural resistance to developing key pathological features of CKD, such as tubulointerstitial fibrosis and inflammation. There have been attempts to overcome these barriers by using multiple concentrations of adenine-supplemented diets or by performing prolonged experiments up to 20 weeks. Here, we demonstrate that SKH1 Elite mice develop clinically relevant CKD phenotypes (e.g., polyuria, proteinuria, inflammation, and renal fibrosis) over the course of only 6 weeks of low-dose (0.15%) adenine supplementation. As a docile, immunocompetent, and hairless strain, SKH1 Elite mice offer several logistical advantages over C57BL/6 mice, including ease of handling and the ability to study dermal conditions, which are often secondary to CKD.

摘要

常用的腺嘌呤诱导慢性肾脏病(CKD)小鼠模型通常采用C57BL/6小鼠;然而,该品系由于对发展CKD的关键病理特征(如肾小管间质纤维化和炎症)具有天然抗性而存在固有局限性。已经尝试通过使用多种浓度的添加腺嘌呤的饮食或进行长达20周的长期实验来克服这些障碍。在此,我们证明,在仅6周的低剂量(0.15%)腺嘌呤补充过程中,SKH1 Elite小鼠就会出现临床相关的CKD表型(如多尿、蛋白尿、炎症和肾纤维化)。作为一种温顺、具有免疫活性的无毛品系,SKH1 Elite小鼠相对于C57BL/6小鼠具有一些后勤优势,包括易于处理以及能够研究通常继发于CKD的皮肤状况。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3112/11726765/7f255c82582d/cells-13-02117-g001.jpg

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