Abstract
Mycotoxins, especially deoxynivalenol (DON), are common contaminants of food and feed, which also has serious threaten to human health and livestock production. Moreover, DON severely impair intestinal epithelial barrier function. Therefore, it is necessary to investigate the mechanism of intestinal epithelial cell injury induced by DON. Here, intestinal porcine enterocyte cell (IPEC-J2) was incubated with 200ng/ml or 2000ng/ml DON for 6h, then lncRNA sequencing, metabolomics and proteomics were applied. Combined with long coding transcriptomics, and proteomics, 200ng/ml DON treatment (LDON group) significantly upregulated ribosome biogenesis in eukaryotes, spliceosome, and ubiquitin mediated proteolysis, RNA transport, and downregulated metabolic pathways in IPEC-J2, 2000ng/ml of DON treatment (HDON group) significantly upregulated ribosome biogenesis in eukaryotes, and spliceosome, and downregulated base excision repair, cell cycle, DNA replication, homologous recombination, and mismatch repair in IPEC-J2. Combined with long coding transcriptomics, and proteomics, as compared with LDON group, HDON group significantly upregulated adherens junction, hippo signaling pathway, and pathways in cancer, and downregulated DNA replication pathways in IPEC-J2. In metabolomics, LDON group and HDON group was mainly downregulated biosynthesis of unsaturated fatty acids, and fatty acid metabolism. These results provide a new insight to prevent and treat DON induced intestinal epithelial cell injury.
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