现代食品科技2025，Vol.41Issue(1)：8-16,9.DOI:10.13982/j.mfst.1673-9078.2025.1.1181
呕吐毒素致HK2细胞氧化应激的作用机制
Mechanism for Vomitoxin-induced Oxidative Stress in HK2 Cells
摘要
Abstract
The mechanism of action of deoxynivalenol(DON)on oxidative stress in human renal tubular epithelial cells(Human Kidney-2,HK2)was explored in this article.DON cytotoxicity was assessed using the MTT assay,and the expression levels of apoptosis-regulating proteins-including Bax,Bcl-2,Caspase-2,Caspase-3,Caspase-6,Caspase-8,and Caspase-9-was measured by Western blotting.Transcriptome sequencing(RNA-seq)analyzed the genome-wide expression profile of HK2 cells following 24-hour DON exposure.DON exposure elevated LDH,MDA,and ROS levels in HK2 cells,while reducing antioxidant indicators such as SOD and GSH and increasing inflammatory markers IL-6,IL-1β,and TNF-α.Bax and caspase protein expressions were upregulated,while Bcl-2 protein expression was downregulated.Transcriptome analysis identified 5 962 differentially expressed genes after exposure to 40 µmol/L DON,with 2 813 upregulated and 3 149 downregulated.Protein levels aligned with gene expression profiles.DON induces oxidative stress and nephrotoxicity in HK2 cells,affecting renal function and metabolism through signaling pathways,including Caspase,MAPK,and PI3K-Akt.These findings offer a theoretical basis for the regulation of DON-induced nephrotoxicity.关键词
呕吐毒素/氧化胁迫/炎症反应/细胞凋亡/差异基因分析Key words
vomitoxin/oxidative stress/inflammatory reactions/apoptosis/differential gene analysis引用本文复制引用
焦禄,张百刚,李苏冰,李阳,付炳钢..呕吐毒素致HK2细胞氧化应激的作用机制[J].现代食品科技,2025,41(1):8-16,9.基金项目
国家自然科学基金项目(31760495) （31760495）
甘肃省自然科学基金项目(18JR3RA136) （18JR3RA136）
