Weaning causes redox dyshomeostasis in piglets, which leads to hepatic oxidative damage. Microbe-derived antioxidants (MA) have great potential for anti-oxidation. This study aimed to investigate changes in hepatic redox system, mitochondrial function and apoptosis after weaning, and effects of MA on growth performance and liver health in weaning piglets. This study consisted of 2 experiments. In the both experiments, piglets were weaned at 21 days of age. In Exp. 1, at 21 (W0), 22 (W1), 25 (W4), 28 (W7), and 35 (W14) days of age, 6 piglets were slaughtered at each timepoint. In Exp. 2, piglets were divided into 2 groups: one received MA gavage (MA) and the other received saline gavage (CON). At 25 days of age, 6 piglets from each group were sacrificed. In Exp. 1, weaning caused growth inhibition and liver developmental retardation from W0 to W4. The mRNA sequencing between W0 and W4 revealed that pathways related to “regulation of apoptotic process” and “reactive oxygen species metabolic process” were enriched. Further study showed that weaning led to higher hepatic content of reactive oxygen species (ROS), H2O2 and O2−. Weaning enhanced mitochondrial fission and suppressed their fusion, activated mitophagy, thus triggering cell apoptosis. In Exp. 2, MA improved growth performance of piglets with higher average daily gain (ADG) and average daily feed intake (ADFI). The hepatic ROS, as well as products of oxidative damage malonaldehyde (MDA) and 8-hydroxy-2′-deoxyguanosine (8-OHdG) in the MA group decreased significantly than that of the CON group. The MA elevated mitochondrial membrane potential, increased activity of mitochondrial respiratory chain complexes (MRC) I and IV, enhanced mitochondrial fusion and reduced mitophagy, thus decreasing cell apoptosis. The present study showed that MA improved the growth performance of weaning piglets and reversed weaning-induced oxidative damage, mitochondrial dysfunction, and apoptosis. Our results suggested that MA had promising prospects for maintaining liver health in weaning piglets and provided a reference for studies of liver diseases in humans.

中文翻译：

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微生物来源的抗氧化剂对断奶仔猪生长性能、肝脏氧化应激、线粒体功能和细胞凋亡的影响


断奶会导致仔猪氧化还原稳态失调，从而导致肝脏氧化损伤。微生物衍生的抗氧化剂 （MA） 具有巨大的抗氧化潜力。本研究旨在探讨断奶后肝脏氧化还原系统、线粒体功能和细胞凋亡的变化，以及 MA 对断奶仔猪生长性能和肝脏健康的影响。本研究包括 2 个实验。在这两个实验中，仔猪在 21 日龄时断奶。在实验 1 中，在 21 （W0）、22 （W1）、25 （W4）、28 （W7） 和 35 （W14） 日龄时，每个时间点屠宰 6 头仔猪。在实验 2 中，仔猪分为 2 组：一组接受 MA 管饲法 （MA），另一组接受盐水管饲法 （CON）。在 25 日龄时，每组处死 6 头仔猪。在实验 1 中，脱机导致生长抑制和从 W0 到 W4 的肝脏发育迟缓。W0 和 W4 之间的 mRNA 测序显示，与“凋亡过程的调节”和“活性氧代谢过程”相关的通路富集。进一步的研究表明，脱机导致肝脏活性氧 （ROS）、H2O2 和 O2− 含量升高。脱机增强了线粒体裂变并抑制了它们的融合，激活了线粒体自噬，从而触发了细胞凋亡。在实验 2 中，MA 以更高的平均日增重 （ADG） 和平均日采食量 （ADFI） 改善了仔猪的生长性能。MA 组肝脏 ROS 以及氧化损伤丙二醛 （MDA） 和 8-羟基-2′-脱氧鸟苷 （8-OHdG） 的产物显著低于 CON 组。MA 提高了线粒体膜电位，增加了线粒体呼吸链复合物 （MRC） I 和 IV 的活性，增强了线粒体融合并减少了线粒体自噬，从而减少了细胞凋亡。 本研究表明，MA 改善了断奶仔猪的生长性能，逆转了断奶诱导的氧化损伤、线粒体功能障碍和细胞凋亡。我们的结果表明，MA 在维持断奶仔猪肝脏健康方面具有广阔的前景，为人类肝脏疾病的研究提供了参考。