Selenomethionine Antagonized microRNAs Involved in Apoptosis of Rat Articular Cartilage Induced by T-2 Toxin

T-2 toxin and selenium deficiency are considered important etiologies of Kashin–Beck disease (KBD), although the exact mechanism is still unclear. To identify differentially expressed microRNAs (DE-miRNAs) in articular cartilage rats exposed to selenomethionine (SeMet) supplementation, thirty-six 4-week-old Sprague Dawley were divided into a control group (gavaged with 4% anhydrous ethanol), 100 ng/g·bw/day toxin), + SeMet 0.5 mg/kg·bw/day SeMet), respectively. Toluidine blue staining was performed detect pathological changes cartilage. Three per randomly selected for high-throughput sequencing Target genes DE-miRNAs predicted using miRanda RNAhybrid databases, Gene Ontology Kyoto Encyclopedia Genes Genomes pathway enriched. The network map miRNA-target constructed Cytoscape software. expression profiles miRNAs associated KBD obtained from Expression Omnibus database. Additionally, real-time quantitative PCR (RT-qPCR) verification. demonstrated that damaged effectively alleviated lesions. A total 50 (28 upregulated 22 downregulated) vs. group, 18 (6 12 25 (5 20 identified. Enrichment analysis showed target apoptosis, MAPK TGF-β signaling pathways group. However, apoptosis not significant These results indicated induced whereas supplementation antagonized apoptosis. Apoptosis autophagy occurred simultaneously may inhibit protect Compared GSE186593 dataset, evidence miR-133a-3p involved more abundant. RT-qPCR validation consistent RNA results. Our findings suggested lesions by toxin, most probably played central role process.