Vitamin U alleviates AFB1-induced hepatotoxicity in pregnant and lactating mice by regulating the Nrf2/Hmox1 pathway

IF 2.2 3区 农林科学 Q1 VETERINARY SCIENCES
Chenxi Ling , Shufan Liu , Keqi Meng , Yake Wang , Xuanxuan Zhang , Jiaxin Liu , Xinfeng Li , Kun Liu , Hongyu Deng , Congcong Li
{"title":"Vitamin U alleviates AFB1-induced hepatotoxicity in pregnant and lactating mice by regulating the Nrf2/Hmox1 pathway","authors":"Chenxi Ling ,&nbsp;Shufan Liu ,&nbsp;Keqi Meng ,&nbsp;Yake Wang ,&nbsp;Xuanxuan Zhang ,&nbsp;Jiaxin Liu ,&nbsp;Xinfeng Li ,&nbsp;Kun Liu ,&nbsp;Hongyu Deng ,&nbsp;Congcong Li","doi":"10.1016/j.rvsc.2024.105436","DOIUrl":null,"url":null,"abstract":"<div><div>This study investigated the protective effect of Vitamin U on liver injury induced by aflatoxin B<sub>1</sub> (AFB<sub>1</sub>) in maternal mice. 25 pregnant ICR mice were randomly divided into five groups: the AFB<sub>1</sub> group (AF, 0.3 mg AFB<sub>1</sub>/kg b.w.), the Vitamin U group (U, 50 mg Vitamin U/kg b.w.), the AFB<sub>1</sub> + Vitamin U group (AU, 50 mg Vitamin U /kg b.w. + 0.3 mg AFB<sub>1</sub>/kg b.w.), the control group (DMSO), and the MOCK group (distilled water). They were administered substances by gavage every day for 28 days. Results indicated that exposure to AFB<sub>1</sub> increased the liver index and caused histological disruptions. Elevated serum levels of ALT and ALP were observed, along with a significant increase in liver MDA content and a decrease in GSH-Px and T-SOD levels. Moreover, the Keap1 and Hmox1 gene was downregulated with statistical significance, while the IL1β and TNFα gene were significantly upregulated. Vitamin U was demonstrated by the organized structure of liver cells in tissue slices, effectively reducing liver cell necrosis. This intervention was associated with a significant decrease in serum ALT and ALP activities, as well as a significant decrease in liver MDA content. Additionally, there were significant increases in liver T-SOD and GSH-Px levels, along with upregulation of mRNA and protein expression of Nfr2, Hmox1 and Keap1, and downregulation of mRNA expression of the IL1β gene. In summary, Vitamin U mitigated oxidative stress-induced liver injury by modulating the Nrf2/Hmox1 signaling pathway and inflammatory factors affected by AFB<sub>1</sub>.</div></div>","PeriodicalId":21083,"journal":{"name":"Research in veterinary science","volume":"180 ","pages":"Article 105436"},"PeriodicalIF":2.2000,"publicationDate":"2024-10-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Research in veterinary science","FirstCategoryId":"97","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0034528824003035","RegionNum":3,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"VETERINARY SCIENCES","Score":null,"Total":0}
引用次数: 0

Abstract

This study investigated the protective effect of Vitamin U on liver injury induced by aflatoxin B1 (AFB1) in maternal mice. 25 pregnant ICR mice were randomly divided into five groups: the AFB1 group (AF, 0.3 mg AFB1/kg b.w.), the Vitamin U group (U, 50 mg Vitamin U/kg b.w.), the AFB1 + Vitamin U group (AU, 50 mg Vitamin U /kg b.w. + 0.3 mg AFB1/kg b.w.), the control group (DMSO), and the MOCK group (distilled water). They were administered substances by gavage every day for 28 days. Results indicated that exposure to AFB1 increased the liver index and caused histological disruptions. Elevated serum levels of ALT and ALP were observed, along with a significant increase in liver MDA content and a decrease in GSH-Px and T-SOD levels. Moreover, the Keap1 and Hmox1 gene was downregulated with statistical significance, while the IL1β and TNFα gene were significantly upregulated. Vitamin U was demonstrated by the organized structure of liver cells in tissue slices, effectively reducing liver cell necrosis. This intervention was associated with a significant decrease in serum ALT and ALP activities, as well as a significant decrease in liver MDA content. Additionally, there were significant increases in liver T-SOD and GSH-Px levels, along with upregulation of mRNA and protein expression of Nfr2, Hmox1 and Keap1, and downregulation of mRNA expression of the IL1β gene. In summary, Vitamin U mitigated oxidative stress-induced liver injury by modulating the Nrf2/Hmox1 signaling pathway and inflammatory factors affected by AFB1.
维生素 U 通过调节 Nrf2/Hmox1 通路减轻 AFB1 诱导的妊娠小鼠和哺乳小鼠肝毒性
本研究探讨了维生素 U 对黄曲霉毒素 B1(AFB1)引起的母鼠肝损伤的保护作用。25 只怀孕的 ICR 小鼠被随机分为五组:AFB1 组(AF,0.3 毫克 AFB1/千克体重)、维生素 U 组(U,50 毫克维生素 U/千克体重)、AFB1 + 维生素 U 组(AU,50 毫克维生素 U/千克体重 + 0.3 毫克 AFB1/千克体重)、对照组(二甲基亚砜)和 MOCK 组(蒸馏水)。它们每天灌胃给药,连续 28 天。结果表明,暴露于 AFB1 会增加肝脏指数并导致组织学破坏。观察到血清 ALT 和 ALP 水平升高,肝脏 MDA 含量显著增加,GSH-Px 和 T-SOD 水平下降。此外,Keap1 和 Hmox1 基因的下调具有统计学意义,而 IL1β 和 TNFα 基因则明显上调。组织切片中肝细胞的有序结构表明,维生素 U 能有效减少肝细胞坏死。这种干预与血清 ALT 和 ALP 活性的显著降低以及肝脏 MDA 含量的显著降低有关。此外,肝脏中的 T-SOD 和 GSH-Px 含量也有明显增加,Nfr2、Hmox1 和 Keap1 的 mRNA 和蛋白表达上调,IL1β 基因的 mRNA 表达下调。总之,维生素U通过调节Nrf2/Hmox1信号通路和受AFB1影响的炎症因子,减轻了氧化应激诱导的肝损伤。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
Research in veterinary science
Research in veterinary science 农林科学-兽医学
CiteScore
4.40
自引率
4.20%
发文量
312
审稿时长
75 days
期刊介绍: Research in Veterinary Science is an International multi-disciplinary journal publishing original articles, reviews and short communications of a high scientific and ethical standard in all aspects of veterinary and biomedical research. The primary aim of the journal is to inform veterinary and biomedical scientists of significant advances in veterinary and related research through prompt publication and dissemination. Secondly, the journal aims to provide a general multi-disciplinary forum for discussion and debate of news and issues concerning veterinary science. Thirdly, to promote the dissemination of knowledge to a broader range of professions, globally. High quality papers on all species of animals are considered, particularly those considered to be of high scientific importance and originality, and with interdisciplinary interest. The journal encourages papers providing results that have clear implications for understanding disease pathogenesis and for the development of control measures or treatments, as well as those dealing with a comparative biomedical approach, which represents a substantial improvement to animal and human health. Studies without a robust scientific hypothesis or that are preliminary, or of weak originality, as well as negative results, are not appropriate for the journal. Furthermore, observational approaches, case studies or field reports lacking an advancement in general knowledge do not fall within the scope of the journal.
文献相关原料
公司名称 产品信息 采购帮参考价格
上海源叶 Vitamin U
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信