膳食中补充阿魏酸可提高抗氧化能力,缓解敌草快挑战仔猪肝细胞的脓毒症。

IF 6.3 Q1 AGRICULTURE, DAIRY & ANIMAL SCIENCE
Junqiu Luo, Xiu Wu, Daiwen Chen, Bing Yu, Jun He
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引用次数: 0

摘要

背景氧化应激会严重影响仔猪的生长性能和肝脏功能。阿魏酸(FA)是一种抗氧化剂,然而,人们对阿魏酸在调节敌草快诱导的仔猪氧化应激中的作用和机制知之甚少。本研究旨在探讨敌草快挑战下 FA 对仔猪生长性能和抗氧化能力的影响:32头健康的DLY(杜洛克×兰德拉克×约克夏)仔猪(13.24 ± 0.19 kg)被随机分配到两种日粮中,其中一种日粮包括0或4 g/kg的阿魏,持续14 d;第15 d,所有猪腹腔注射敌草快或无菌生理盐水:结果:日粮中添加阿魏酸(FA)可显著提高仔猪的平均日增重(ADG),降低饲料报酬比(F/G)。补充阿魏酸可降低敌草快挑战仔猪的血清天冬氨酸氨基转移酶(AST)和丙氨酸氨基转移酶(ALT)活性。此外,灌注敌草快增加了肝脏中活性氧自由基(ROS)的水平,降低了总超氧化物歧化酶(T-SOD)和谷胱甘肽过氧化物酶(GSH-Px)的活性、总抗氧化能力(T-AOC),并增加了肝脏和血清中丙二醛(MDA)的含量。补充 FA 能明显提高 T-AOC 和 T-SOD 活性,降低 MDA 和 ROS 水平。FA 下调了挑战敌草快仔猪肝脏中 Keap1 的基因和蛋白表达,上调了 Nrf2 和 HO-1 的蛋白表达。重要的是,敌草快挑战增加了晚期细胞凋亡的比例,提高了血清中IL-1β、IL-18和乳酸脱氢酶(LDH)的水平,并上调了肝脏中热凋亡相关基因的表达。补充足量脂肪酸可降低晚期细胞凋亡的比例,并下调 Caspase-1 的 mRNA 表达。因此,在敌草快挑战下,添加FA可降低IL-1β、IL-18和LDH的浓度:结论:敌草快诱导的氧化应激降低了仔猪的生长性能并损害了其肝功能。结论:敌草快诱导的氧化应激降低了仔猪的生长性能并损害了其肝脏功能。膳食中添加足量脂肪酸可提高抗氧化能力并降低肝细胞脓毒症的程度,从而减轻肝脏的氧化损伤并减轻敌草快对仔猪生长性能的影响。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Dietary ferulic acid supplementation enhances antioxidant capacity and alleviates hepatocyte pyroptosis in diquat challenged piglets.

Background: Oxidative stress significantly impacts growth performance and liver function in piglets. Ferulic acid (FA) works as an antioxidant, however, the role and mechanism of FA in the regulation of diquat-induced oxidative stress in piglets are less known. This study was designed to investigate the effects of FA on growth performance and antioxidant capacity in piglets with diquat challenge.

Methods: Thirty-two healthy DLY (Duroc × Landrace × Yorkshire) piglets (13.24 ± 0.19 kg) were randomly divided into one of two diets including 0 or 4 g/kg FA for 14 d. On d 15, all pigs were intraperitoneally injected diquat or sterile saline.

Results: Dietary supplementation with ferulic acid (FA) significantly improved the average daily gain (ADG) and decreased feed-gain ratio (F/G) of piglets. Here, dietary FA supplementation reduced serum aspartate aminotransferase (AST), alanine aminotransferase (ALT) activities in diquat challenged piglets. Furthermore, diquat infusion increased reactive oxygen radicals (ROS) level in liver, decreased the activities of total superoxide dismutase (T-SOD) and glutathione peroxidase (GSH-Px), total antioxidant capacity (T-AOC) and increased malondialdehyde (MDA) content in the liver and serum. Supplementation with FA significantly increased T-AOC and T-SOD activities and decreased MDA and ROS levels. FA down-regulated gene and protein expression of Keap1, and up-regulated protein expression of Nrf2 and HO-1 in the liver of piglets with diquat challenge. Importantly, diquat challenge increased the ratio of late apoptosis, increased serum levels of IL-1β, IL-18 and lactate dehydrogenase (LDH), and up-regulated pyroptosis-related genes in the liver. FA supplementation reduced the ratio of late apoptosis and down-regulated mRNA expression of Caspase-1. Accordingly, FA addition reduced concentration of IL-1β, IL-18, and LDH under diquat challenge.

Conclusions: Diquat-induced oxidative stress reduced growth performance and impaired liver function in piglets. Dietary FA supplementation enhanced the antioxidant capacity and reduced the degree of hepatocyte pyroptosis, thereby alleviating the oxidative damage in the liver and mitigating the impact of diquat on growth performance of piglets.

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