该文探究了呕吐毒素（Deoxynivalenol, DON）对人肾小管上皮细胞（Humankideny-2, HK2）氧化应激的作用机制。通过MTT法测定DON的细胞毒性，Western blotting检测细胞凋亡蛋白Bax、Bcl-2、Caspase-2、Caspase-3、Caspase-6、Caspase-8和Caspase-9的表达水平。利用转录组测序技术（RNA-seq）研究了DON染毒24 h诱导的HK2细胞基因组表达情况，并进行差异表达基因GO与KEGG富集分析。结果表明，DON使HK2细胞LDH、MDA和ROS水平上升，SOD和GSH等抗氧化指标下降；IL-6、IL-1β和TNF-α等炎症指标升高。Bax和caspase蛋白表达上调，Bcl-2蛋白表达下调。转录组测序表明，40 μmol/L DON诱导的差异表达基因共有5 962个，其中上调表达的基因有2 813个，下调表达的基因有3 149个。综上所述，蛋白水平与基因谱表达趋势一致，DON对HK2细胞具有毒性作用，诱导HK2细胞氧化应激，通过Caspase、MAPK和PI3K-Akt等信号通路影响肾功能与代谢，为DON肾毒性作用和相关机制的调控提供理论依据。

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.

国家自然科学基金项目（31760495）；甘肃省自然科学基金项目（18JR3RA136）