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雏鹌鹑中伏马菌素 B 肾毒性的病理学和分子机制的初步研究。

A preliminary study on the pathology and molecular mechanism of fumonisin B nephrotoxicity in young quails.

机构信息

College of Life Science and Engineering, Foshan University, Foshan, Guangdong, 528231, People's Republic of China.

出版信息

Environ Sci Pollut Res Int. 2023 Nov;30(53):114438-114451. doi: 10.1007/s11356-023-30291-4. Epub 2023 Oct 20.

DOI:10.1007/s11356-023-30291-4
PMID:37858030
Abstract

Fumonisin B (FB) is a widely present mycotoxin that accumulates in biological systems and poses a health risk to animals. However, few studies have reported the molecular mechanism by which FB induces nephrotoxicity. The aim of this study was to assess the extent of nephrotoxicity during FB exposure and the possible molecular mechanisms behind it. Therefore, 180 young quails were equally divided into two groups. The control group was fed typical quail food, while the experimental group was fed quail food containing 30 mg·kg FB. Various parameters were assessed, which included histopathological, ultrastructural changes, levels of biochemical parameters, oxidative indicators, inflammatory factors, possible target organelles mitochondrial and endoplasmic reticulum (ER)-related factors, nuclear xenobiotic receptors (NXR) response, and cytochrome P450 system (CYP450s)-related factors in the kidneys on days 14, 28, and 42. The results showed that FB can induce oxidative stress through NXR response and disorder of the CYP450s system, leading to mitochondrial dysfunction and ER stress, promoting the expression of inflammatory factors (including IL-1β, IL-6, and IL-8) and causing kidney damage. This study elucidated the possible molecular mechanism by which FB induces nephrotoxicity in young quails.

摘要

伏马菌素 B(FB)是一种广泛存在的真菌毒素,会在生物系统中积累,对动物的健康构成威胁。然而,目前很少有研究报道 FB 诱导肾毒性的分子机制。本研究旨在评估 FB 暴露期间肾毒性的程度及其可能的分子机制。因此,将 180 只幼鹌鹑平均分为两组。对照组喂食典型的鹌鹑饲料,实验组喂食含有 30mg·kg FB 的鹌鹑饲料。在第 14、28 和 42 天评估了各种参数,包括组织病理学、超微结构变化、生化参数水平、氧化指标、炎症因子、可能的靶细胞器线粒体和内质网(ER)相关因素、核异源受体(NXR)反应以及肾脏中的细胞色素 P450 系统(CYP450s)相关因素。结果表明,FB 可以通过 NXR 反应和 CYP450s 系统的紊乱诱导氧化应激,导致线粒体功能障碍和 ER 应激,促进炎症因子(包括 IL-1β、IL-6 和 IL-8)的表达,导致肾脏损伤。本研究阐明了 FB 诱导幼鹌鹑肾毒性的可能分子机制。

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