Yu Chengbing, Luo Yuxiao, Shen Cheng, Luo Zhen, Zhang Hongcai, Zhang Jing, Xu Weina, Xu Jianxiong
Shanghai Key Laboratory of Veterinary Biotechnology, School of Agriculture and Biology, Shanghai Jiao Tong University, Shanghai, 200240, China.
J Anim Sci Biotechnol. 2024 Oct 2;15(1):128. doi: 10.1186/s40104-024-01088-3.
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), HO and O. 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.
断奶会导致仔猪氧化还原稳态失衡，进而引发肝脏氧化损伤。微生物源抗氧化剂（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。在两个实验中，仔猪均在21日龄断奶。在实验1中，在21日龄（W0）、22日龄（W1）、25日龄（W4）、28日龄（W7）和35日龄（W14）时，每个时间点宰杀6头仔猪。在实验2中，仔猪分为2组：一组接受MA灌胃（MA组），另一组接受生理盐水灌胃（CON组）。在25日龄时，每组宰杀6头仔猪。
在实验1中，从W0到W4，断奶导致生长抑制和肝脏发育迟缓。W0和W4之间的mRNA测序显示，与“凋亡过程调控”和“活性氧代谢过程”相关的通路富集。进一步研究表明，断奶导致肝脏活性氧（ROS）、HO和O含量升高。断奶增强了线粒体分裂并抑制其融合，激活了线粒体自噬，从而引发细胞凋亡。在实验2中，MA提高了仔猪的生长性能，平均日增重（ADG）和平均日采食量（ADFI）更高。MA组肝脏ROS以及氧化损伤产物丙二醛（MDA）和8-羟基-2'-脱氧鸟苷（8-OHdG）均显著低于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，逆转了断奶引起的氧化损伤、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前景，并为人类肝脏疾病的研究提供了参考。
