Dietary Tributyrin Attenuates Intestinal Inflammation, Enhances Mitochondrial Function, and Induces Mitophagy in Piglets Challenged with Diquat
Dietary Tributyrin Attenuates Intestinal Inflammation, Enhances Mitochondrial Function, and Induces Mitophagy in Piglets Challenged with Diquat
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日粮三丁酸甘油酯可减轻敌草快挑战仔猪的肠道炎症、增强线粒体功能并诱导线粒体自噬
DOI：
10.1021/acs.jafc.8b06208
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发表时间：
2019
影响因子：
6.1
通讯作者：
Caihong Hu
中科院分区：
文献类型：
--
作者：
Chunchun Wang;Shuting Cao;Qianhui Zhang;Zhuojun Shen;Jie Feng;Qihua Hong;Jianjun Lu;Fei Xie;Yan Peng;Caihong Hu
该研究评估了三丁酸甘油酯形式的丁酸对敌草快攻击的猪的氧化应激、炎症和线粒体功能的影响。将 24 头断奶猪按照 2 × 2 因子排列分配至 4 个处理组，主要效果是补充三丁酸甘油酯和敌草快挑战。结果表明，补充三丁酸甘油酯增加了敌草快攻击猪的平均日增重和平均日采食量（P<0.05）。三丁酸甘油酯可提高敌草快攻击猪的总抗氧化能力和超氧化物歧化酶活性（P<0.05），降低丙二醛含量（P<0.05），增加铜锌超氧化物歧化酶和含锰超氧化物歧化酶的mRNA水平（P<0.05）。三丁酸甘油酯缓解（P<0.05）肠道炎症，这反映在肠道中肿瘤坏死因子-α、干扰素-γ和白细胞介素-6的mRNA丰度降低。三丁酸甘油酯可降低（P<0.05）血清二胺氧化酶活性和D-乳酸含量，增加（P<0.05）跨上皮电阻，减少右旋糖酐的细胞旁通量（4kDa），并阻止敌草快诱导的claudin-1、occludin和zonula occlusionns-1表达的减少（P<0.05）。三丁酸甘油酯可减轻（P<0.05）敌草快诱导的线粒体功能障碍，表现为降低活性氧、增加线粒体膜电位和增加三磷酸腺苷含量。此外，三丁酸甘油酯可增加（P < 0.05）线粒体自噬蛋白（PTEN 诱导的推定激酶 1 和 Parkin）的表达以及肠道中轻链 3-II 与轻链 3-I 的比率。总的来说，三丁酸甘油酯可以减轻敌草快攻击猪的氧化应激和肠道炎症，改善线粒体功能，并诱导线粒体自噬。
The study evaluated the effects of butyric acid, in the form of tributyrin on the oxidative stress, inflammation, and mitochondrial function in diquat-challenged pigs. Twenty-four weaned pigs were allocated to four treatments in a 2 × 2 factorial arrangement with the main effects of tributyrin supplementation and diquat challenge. The results showed that supplemental tributyrin increased (P< 0.05) average daily gain and average daily feed intake of diquat-challenged pigs. Tributyrin elevated (P< 0.05) the activities of total antioxidant capacity and superoxide dismutase, reduced (P< 0.05) malondialdehyde content, and increased (P< 0.05) mRNA levels of copper and zinc superoxide dismutase and manganese-containing superoxide dismutase of diquat-challenged pigs. Tributyrin relieved (P< 0.05) intestinal inflammation reflected by decreased mRNA abundances of tumor necrosis factor-α, interferon-γ, and interleukin-6 in the intestine. Tributyrin reduced (P< 0.05) serum diamine oxidase activity andd-lactate content, increased (P< 0.05) transepithelial electrical resistance, decreased paracellular flux of dextran (4 kDa), and prevented the diquat-induced decrease (P< 0.05) in the expressions of claudin-1, occludin, and zonula occludens-1. Tributyrin alleviated (P< 0.05) diquat-induced mitochondrial dysfunction shown by lowered reactive oxygen species, increased mitochondrial membrane potential, and increased adenosine triphosphate content. Furthermore, tributyrin increased (P< 0.05) expressions of mitophagy proteins (PTEN-induced putative kinase 1 and Parkin), and ratio of light chain 3-II to light chain 3-I in intestine. Collectively, tributyrin attenuated oxidative stress and intestinal inflammation, improved mitochondrial function, and induced mitophagy in diquat-challenged pigs.