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<p>Aflatoxin B1 (AFB1), a common feed contaminant, causes substantial economic losses in animal husbandry and threatens reproductive health. This study investigated the toxic mechanisms of AFB1 on bovine endometrial epithelial cells using in vitro experiments. Treatment with 5&#xa0;μg/mL AFB1 for 24&#xa0;h significantly inhibited cell proliferation and induced apoptosis, indicated by a reduced EdU-positive rate and increased Bax/Bcl-2 ratio and Caspase-3 expression. Transcriptome sequencing identified 810 differentially expressed mRNAs and 88 upregulated lncRNAs, which were primarily enriched in calcium signaling, oxytocin, and GnRH pathways. Experimental validation confirmed that AFB1 elevated intracellular Ca<sup>2</sup>⁺ levels, dysregulated calcium-related protein expression, and disrupted mitochondrial membrane potential. Further analysis suggested that lncRNAs such as MSTRG.32635 may perturb cellular homeostasis by modulating calcium signaling–associated genes. These findings elucidate a novel mechanism wherein AFB1 impairs endometrial cell function via an lncRNA–mRNA network that interferes with calcium signaling, offering potential targets for the prevention and treatment of AFB1-induced reproductive toxicity.</p>

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Aflatoxin B1 interferes with lncRNA-mRNA network to inhibit proliferation of bovine endometrial epithelial cells

  • 期刊论文

  • 发表日期：

    2025年12月27日

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  • Yin-Yin Li,
  • Yue Bai,
  • Yu-Mei Chen Yan,
  • Pei-Yu Dong,
  • Min Zhang,
  • Xi-Feng Zhang,
  • Yan-Ni Feng

摘要

Aflatoxin B1 (AFB1), a common feed contaminant, causes substantial economic losses in animal husbandry and threatens reproductive health. This study investigated the toxic mechanisms of AFB1 on bovine endometrial epithelial cells using in vitro experiments. Treatment with 5 μg/mL AFB1 for 24 h significantly inhibited cell proliferation and induced apoptosis, indicated by a reduced EdU-positive rate and increased Bax/Bcl-2 ratio and Caspase-3 expression. Transcriptome sequencing identified 810 differentially expressed mRNAs and 88 upregulated lncRNAs, which were primarily enriched in calcium signaling, oxytocin, and GnRH pathways. Experimental validation confirmed that AFB1 elevated intracellular Ca2⁺ levels, dysregulated calcium-related protein expression, and disrupted mitochondrial membrane potential. Further analysis suggested that lncRNAs such as MSTRG.32635 may perturb cellular homeostasis by modulating calcium signaling–associated genes. These findings elucidate a novel mechanism wherein AFB1 impairs endometrial cell function via an lncRNA–mRNA network that interferes with calcium signaling, offering potential targets for the prevention and treatment of AFB1-induced reproductive toxicity.