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<p>Palmitic acid (PA), the most abundant saturated fatty acid in bovine blood, serves not only as an important energy precursor but also induces cellular dysfunction when in excess. This study aimed to elucidate the mechanisms underlying PA-induced mammary gland injury and to identify potential therapeutic strategies for improving mammary health and milk quality. In this study, the STAT3 signaling pathway was significantly downregulated, apoptosis was upregulated, and lipid metabolism was dysregulated in the mammary glands during ketosis, a typical fatty acid surfeit situation. To establish a direct causal role of PA and STAT3, we employed an <i>in vitro</i> MAC-T cell model, where exogenous PA treatment recapitulated the mammary injury phenotype observed <i>in vivo.</i> Furthermore, treatment with Colivelin, a STAT3 activator, alleviated PA-induced apoptosis and fatty acid oxidation impairment in bovine mammary epithelial cells. Cleavage under targets and tagmentation analysis revealed that PA treatment suppressed the binding of STAT3 to the <i>CPT1A</i> promoter. <i>CPT1A</i> knockdown mitigated the protective effects of Colivelin against PA-induced lipotoxicity. These findings suggest that excessive PA impairs fatty acid oxidation in mammary cells through the inhibition of STAT3 activity, thereby contributing to mammary gland injury and reduced milk yield in dairy cows.</p>

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STAT3 suppresses palmitic acid-induced apoptosis and fatty acid oxidation dysfunction in bovine mammary epithelial cells by transcriptionally activating CPT1A

  • 期刊论文

  • 发表日期：

    2026年5月7日

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  • Moli Li,
  • Yihui Huo,
  • Shiquan Zhu,
  • Qiqi Cao,
  • Jiangchun Wan,
  • Yuanqiu Li,
  • Hayley Pitts,
  • Derek Nolan,
  • Juan J. Loor,
  • Chuang Xu

摘要

Palmitic acid (PA), the most abundant saturated fatty acid in bovine blood, serves not only as an important energy precursor but also induces cellular dysfunction when in excess. This study aimed to elucidate the mechanisms underlying PA-induced mammary gland injury and to identify potential therapeutic strategies for improving mammary health and milk quality. In this study, the STAT3 signaling pathway was significantly downregulated, apoptosis was upregulated, and lipid metabolism was dysregulated in the mammary glands during ketosis, a typical fatty acid surfeit situation. To establish a direct causal role of PA and STAT3, we employed an in vitro MAC-T cell model, where exogenous PA treatment recapitulated the mammary injury phenotype observed in vivo. Furthermore, treatment with Colivelin, a STAT3 activator, alleviated PA-induced apoptosis and fatty acid oxidation impairment in bovine mammary epithelial cells. Cleavage under targets and tagmentation analysis revealed that PA treatment suppressed the binding of STAT3 to the CPT1A promoter. CPT1A knockdown mitigated the protective effects of Colivelin against PA-induced lipotoxicity. These findings suggest that excessive PA impairs fatty acid oxidation in mammary cells through the inhibition of STAT3 activity, thereby contributing to mammary gland injury and reduced milk yield in dairy cows.