Effects of microbe-derived antioxidants on growth performance, hepatic oxidative stress, mitochondrial function and cell apoptosis in weaning piglets.

IF 6.3 Q1 AGRICULTURE, DAIRY & ANIMAL SCIENCE
Chengbing Yu, Yuxiao Luo, Cheng Shen, Zhen Luo, Hongcai Zhang, Jing Zhang, Weina Xu, Jianxiong Xu
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Abstract

Background: 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.

Methods: 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.

Results: 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.

Conclusions: 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.

微生物衍生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
背景:断奶会造成仔猪体内氧化还原失衡,从而导致肝脏氧化损伤。微生物衍生抗氧化剂(MA)在抗氧化方面具有巨大潜力。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:本研究包括两项实验。在这两项实验中,仔猪均在 21 日龄断奶。在实验 1 中,21(W0)日龄、22(W1)日龄、25(W4)日龄、28(W7)日龄和 35(W14)日龄时,每个时间点屠宰 6 头仔猪。在实验 2 中,仔猪被分为两组:一组接受 MA 灌胃(MA),另一组接受生理盐水灌胃(CON)。每组 6 头仔猪在 25 日龄时被处死:在实验 1 中,从 W0 到 W4,断奶会导致生长抑制和肝脏发育迟缓。对W0和W4的mRNA测序发现,与 "细胞凋亡过程调控 "和 "活性氧代谢过程 "相关的通路被富集。进一步研究表明,断奶导致肝脏活性氧(ROS)、H2O2 和 O2-含量增加。断奶增强了线粒体裂变,抑制了线粒体融合,激活了有丝分裂,从而引发了细胞凋亡。在实验 2 中,MA 改善了仔猪的生长性能,提高了平均日增重(ADG)和平均日采食量(ADFI)。MA组的肝脏ROS以及氧化损伤产物丙二醛(MDA)和8-羟基-2'-脱氧鸟苷(8-OHdG)明显低于CON组。MA能提高线粒体膜电位,增加线粒体呼吸链复合物(MRC)I和IV的活性,增强线粒体融合,减少有丝分裂,从而减少细胞凋亡:本研究表明,MA 可改善断奶仔猪的生长性能,逆转断奶诱导的氧化损伤、线粒体功能障碍和细胞凋亡。我们的研究结果表明,MA 有助于维持断奶仔猪的肝脏健康,并为人类肝脏疾病的研究提供了参考。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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