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减轻支链脂肪酸对脂多糖诱导的犊牛小肠上皮细胞炎症反应的影响

Alleviating the Effect of Branched-Chain Fatty Acids on the Lipopolysaccharide-Induced Inflammatory Response in Calf Small Intestinal Epithelial Cells.

作者信息

Zhang Siqi, Yu Qingyuan, Sun Yukun, Zhang Guangning, Zhang Yonggen, Xin Hangshu

机构信息

College of Animal Science and Technology, Northeast Agricultural University, Harbin 150030, China.

出版信息

Antioxidants (Basel). 2025 May 19;14(5):608. doi: 10.3390/antiox14050608.

DOI:10.3390/antiox14050608
PMID:40427489
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12109260/
Abstract

This study examined branched-chain fatty acids (BCFAs)' effects on oxidative stress, energy metabolism, inflammation, tight junction disruption, apoptosis, and Toll-like receptor 4/nuclear factor kappa-B () signaling in lipopolysaccharide (LPS)-induced calf small intestinal epithelial cells (CSIECs). Eight groups were used: a control group, an LPS-induced group, and six BCFA treatment groups (12-methyltridecanoic acid (iso-C14:0), 13-methyltetradecanoic acid (iso-C15:0), 14-methylpentadecanoic acid (iso-C16:0), 15-methylhexadecanoic acid (iso-C17:0), 12-methyltetradecanoic acid (anteiso-C15:0), and 14-methylhexadecanoic acid (anteiso-C17:0)) with LPS. The BCFA pretreatments significantly increased CSIEC activity compared to the LPS-induced group, with iso-C14:0 showing the highest activity (89.73%). BCFA reduced Reactive Oxygen Species (ROS) generation and malondialdehyde (MDA) levels and improved the superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase (CAT) activities and glutathione (GSH) levels. Iso-C16:0 optimized total antioxidant capacity (T-AOC). BCFA enhanced the mitochondrial membrane potential, Adenosine Triphosphate (ATP) enzyme activity, and ATP content, with iso-C14:0 increasing ATP by 27.01%. BCFA downregulated interleukin (), , tumor necrosis factor ()-, and interferon ()- gene expression, reduced IL-6 levels, and increased expression. Myeloid differentiation factor 88 () mRNA levels were reduced. BCFA alleviated Zonula Occludin (), , and decrease and increased Occludin levels. BCFA mitigated LPS-induced increases in and BCL2-Associated X () mRNA levels, reduced and expression, and increased B-Cell Lymphoma-2 () mRNA levels. The Entropy Weight-TOPSIS method was adopted, and it was discovered that iso-C15:0 has the best effect. In summary, BCFA supplementation mitigated oxidative stress and enhanced mitochondrial function. BCFA inhibited signaling pathway overactivation, regulated inflammatory cytokine gene expression, reduced cellular apoptosis, preserved tight junction integrity, and supported barrier function.

摘要

本研究检测了支链脂肪酸（BCFAs）对脂多糖（LPS）诱导的犊牛小肠上皮细胞（CSIECs）氧化应激、能量代谢、炎症、紧密连接破坏、细胞凋亡及Toll样受体4/核因子κB（）信号通路的影响。实验分为八组：对照组、LPS诱导组以及六个BCFA处理组（12 - 甲基十三烷酸（异-C14:0）, 13 - 甲基十四烷酸（异-C15:0）, 14 - 甲基十五烷酸（异-C16:0）, 15 - 甲基十六烷酸（异-C17:0）, 12 - 甲基十四烷酸（anteiso-C15:0）, 14 - 甲基十六烷酸（anteiso-C I7:0））与LPS共同处理组。与LPS诱导组相比，BCFA预处理显著提高了CSIEC活性, 其中异-C14:0活性最高（89.73%）。BCFA降低了活性氧（ROS）生成和丙二醛（MDA）水平，提高了超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GSH-Px）、过氧化氢酶（CAT）活性及谷胱甘肽（GSH）水平。异-C16:0优化了总抗氧化能力（T-AOC）。BCFA增强了线粒体膜电位、三磷酸腺苷（ATP）酶活性及ATP含量，异-C14:0使ATP增加了27.01%。BCFA下调了白细胞介素（）、、肿瘤坏死因子（）-α和干扰素（）-γ基因表达，降低了IL-6水平，增加了表达。髓样分化因子88（）mRNA水平降低。BCFA减轻了闭合蛋白（）、、和的减少，增加了闭合蛋白水平。BCFA减轻了LPS诱导的和BCL2相关X蛋白（）mRNA水平升高，降低了和表达，增加了B细胞淋巴瘤-2（）mRNA水平。采用熵权-TOPSIS法发现异-C15:0效果最佳。综上所述，补充BCFA可减轻氧化应激并增强线粒体功能。BCFA抑制了信号通路过度激活，调节炎症细胞因子基因表达，减少细胞凋亡，维持紧密连接完整性并支持屏障功能。

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