期刊文献+

伏马毒素B_(1)暴露诱导幼龄鹌鹑肝脏损伤及其机制研究

Study on the Liver Damage of Juvenile Quails by Fumonisin B_(1) Exposure and Its Molecular Mechanism
下载PDF
导出
摘要 为评估伏马毒素B_(1)(FB_(1))暴露引起的肝损伤及分子机制,将120只1日龄鹌鹑平均分为2组,对照组喂食正常鹌鹑饲料,试验组喂含有30 mg/kg FB_(1)的鹌鹑饲料,建立FB_(1)亚慢性中毒模型,记录每天鹌鹑体重变化。在FB_(1)暴露14 d、28 d和42 d,采集各组鹌鹑血液和肝脏样本。测定血液生化指标变化,苏木精-伊红(HE)和马松(Masson)染色、透射电镜观察FB1对肝脏组织的影响,检测相关氧化酶及氧化产物的活性或含量变化,RT-qPCR检测Nrf2通路相关因子、线粒体和炎症相关因子的mRNA表达变化。结果表明,FB_(1)暴露组出现肝细胞肿胀,细胞空泡化,明显充血,纤维化等肝损伤现象,血液生化指标谷胱甘肽转氨酶(AST)、γ-谷氨酰转肽酶(γ-GT)和总胆红素(TBIL)显著上升(P<0.05);超氧化物歧化酶(SOD)、过氧化氢酶(CAT)和谷胱甘肽过氧化物酶(GSH-PX)活性显著下降(P<0.05),丙二醛(MDA)含量显著上升(P<0.05);RT-qPCR结果显示线粒体相关因子表达紊乱,SIRT3、SIRT1的mRNA表达量显著降低(P<0.05),RAF1表达显著上升(P<0.05);IL-8、IL-18、Fasl、IL-12β等促炎因子的mRNA表达量显著上升(P<0.05)。表明FB_(1)抑制氧化酶的活性,引起线粒体功能障碍,诱导氧化应激和炎症反应,致使肝脏受损。 The purpose of this study is to evaluate liver damage caused by exposure to fumaroxin(B_(1))and possible molecular mechanisms.1201-day-old quails were divided into two groups on average.The control group was fed normal quail feed,and the experimental group was fed quail feed with 30 mg/kg FB_(1).A model of FB_(1)sub-chronic poisoning was established to record daily quail weight changes.At 14d,28d and 42d,blood and liver samples from each group of quails were collected.Determination of changes in blood biochemical indicators,HE and Masson staining,transmission electron microscopy to observe the effects of FBi on liver tissue,detection of changes in the activities or contents of related oxidases and oxidation products,RT-qPCR detection of Nrf2 pathway-related factors,mitochondrial-related factors and inflammationrelated factors mRNA expression changes were conducted.The results showed that the FB_(1)exposed group had liver cell swelling,cell vacuolization,obvious congestion,fibrosis and other liver damage phenomena,and blood biochemical indicators,glutathione aminotransferase(AST),-glutamyltransferase(-GT)and total bilirubin(TBIL),increased significantly(P<0.05);superoxide dismutase(SOD),catalase(CAT)and glutathione peroxidase(GSH-PX)activities decreased significantly(P<0.05),the content of malondialdehyde(MDA)increased significantly(P<0.05).The RT-qPCR results showed that the expressions of mitochondrial-related factors were disturbed,and the mRNA expressions of SIRT3 and SIRT1 were significantly reduced(P<0.05),and the expression of RAF1 was significantly increased(P<0.05),the mRNA expressions of pro-inflammatory factors such as IL-8,IL-18,Fasl,and IL-12βwas significantly increased(P<0.05).This study showed that FB_(1)inhibits the activity of oxidase,causing mitochondrial dysfunction,which in turn induces oxidative stress and inflammation,and ultimately causes liver damage.This study clarifies the new molecular mechanism of FB-induced hepatotoxicity in young quails,and provides new ideas for the prevention and c
作者 李锦宏 朱虎全 张若凡 李若彬 宋昭猛 刘阳 王凯 曹嫦妤 LI Jin-hong;ZHU Hu-quan;ZHANG Ruo-fan;LI Ruo-bin;SONG Zhao-meng;LIU Yang;WANG Kai;CAO Chang-yu(College of Life Science and Engineering,Foshan University,Foshan,Guangdong,528231,China;College of Food Science and Engineering,Foshan University,Foshan,Guangdong,528231,China)
出处 《动物医学进展》 北大核心 2024年第8期71-77,共7页 Progress In Veterinary Medicine
基金 广东省基础与应用研究基金(2022B1515130003)。
关键词 伏马毒素B_(1) 氧化应激 线粒体功能障碍 炎症 肝毒性 fumarotoxin B_(1) oxidative stress mitochondrial dysfunction inflammation hepatotoxicity
  • 相关文献

参考文献3

二级参考文献9

共引文献8

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部