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壳寡糖通过激活 ERK1/2 介导的 HO-1 和 GSH-Px 基因表达来缓解肉鸡胸肌急性热应激诱导的氧化损伤。

Chitosan oligosaccharides alleviate acute heat stress-induced oxidative damage by activating ERK1/2-mediated HO-1 and GSH-Px gene expression in breast muscle of broilers.

机构信息

Department of Animal Science, College of Coastal Agriculture Sciences, Guangdong Ocean University, Zhanjiang, Guangdong 524-088, P.R. China.

Department of Animal Science, College of Coastal Agriculture Sciences, Guangdong Ocean University, Zhanjiang, Guangdong 524-088, P.R. China.

出版信息

Poult Sci. 2022 Jan;101(1):101515. doi: 10.1016/j.psj.2021.101515. Epub 2021 Oct 7.

DOI:10.1016/j.psj.2021.101515
PMID:34826744
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8626842/
Abstract

The purpose of this study was to evaluate the effects of chitosan oligosaccharides (COS) on acute heat stress (AHS) induced poor meat quality by alleviating oxidative damage through mitogen-activated protein kinase-nuclear factor-erythroid 2-related factor 2-antioxidant responsive element (MAPK-Nrf2-ARE) signaling pathway. A total of 108 thirty-five-day-old Chinese indigenous broilers (Luhua chicken) was used for this 42-d experiment. The broilers were randomly allocated to 3 treatments: control group (CON), AHS group, and AHS with 400 mg/kg COS supplementation (AHS-C) group. Both CON and AHS groups given the basal diet, and the AHS-C group given the basal diet with 400 mg/kg COS supplementation. On d 42, broilers in the AHS and AHS-C groups treated with AHS (increasing temperature from 24 to 34°C in 2-h and held for another 2-h), and the CON group under normal temperature (24°C). AHS exposure elevated (P < 0.05) body temperature (rectal, comb, eyelids, and feet) of broilers, increased (P < 0.05) breast muscle lightness (L*), drip loss, share force, hydrogen peroxide (HO) scavenging activity, reactive oxygen species (ROS) production, malondialdehyde (MDA) content, and catalase (CAT) activity, however, decreased (P < 0.05) pH, pH, redness (a*), and relative expression of heme oxygenase-1 (HO-1). Compared to the AHS group, dietary COS supplementation increased (P < 0.05) breast muscle pH, pH, and a*, HO scavenging activity, as well as relative expression of HO-1 and glutathione peroxidase (GSH-Px), however, decreased (P < 0.05) drip loss, share force, superoxide anion free radicals (O) scavenging activity, ROS production, and MDA content. It was concluded that AHS impaired meat quality, which may be related to oxidative damage, as evidenced by increasing ROS production, MDA content, and decreasing the relative expression of HO-1. Dietary COS supplementation could effectively elevate the meat quality of broilers exposed to AHS via decreasing ROS production, activating the Nrf2 pathway, and Nrf2-mediated HO-1 and GSH-Px gene expression.

摘要

本研究旨在通过激活丝裂原活化蛋白激酶-核因子红细胞 2 相关因子 2-抗氧化反应元件(MAPK-Nrf2-ARE)信号通路减轻氧化损伤,评估壳寡糖(COS)对急性热应激(AHS)诱导的肉质下降的影响。本试验选用 108 只 35 日龄中国地方鸡种(芦花鸡)进行为期 42 天的试验。将鸡随机分为 3 组:对照组(CON)、AHS 组和 AHS 加 400mg/kg COS 组(AHS-C)。CON 和 AHS 组给予基础日粮,AHS-C 组给予基础日粮加 400mg/kg COS。第 42 天,AHS 和 AHS-C 组的鸡接受 AHS(2h 内将温度从 24°C 升高到 34°C,然后再保持 2h),CON 组在常温(24°C)下饲养。AHS 暴露显著升高(P<0.05)鸡的体温(直肠、鸡冠、眼睑和脚),增加(P<0.05)胸肌亮度(L*)、滴水损失、剪切力、过氧化氢(HO)清除活性、活性氧(ROS)生成、丙二醛(MDA)含量和过氧化氢酶(CAT)活性,但降低(P<0.05)pH、pH、红度(a*)和血红素加氧酶-1(HO-1)的相对表达量。与 AHS 组相比,饲粮中添加 COS 可显著提高(P<0.05)胸肌 pH、pH 和 a*、HO 清除活性以及 HO-1 和谷胱甘肽过氧化物酶(GSH-Px)的相对表达量,降低(P<0.05)滴水损失、剪切力、超氧阴离子自由基(O)清除活性、ROS 生成和 MDA 含量。综上所述,AHS 会损害鸡肉品质,这可能与氧化损伤有关,表现为 ROS 生成增加、MDA 含量降低以及 HO-1 的相对表达量降低。饲粮添加 COS 可通过降低 ROS 生成、激活 Nrf2 通路以及 Nrf2 介导的 HO-1 和 GSH-Px 基因表达,有效提高 AHS 暴露鸡的肌肉品质。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f66/8626842/ed4e2b6189d3/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f66/8626842/89018346b78a/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f66/8626842/51d5fb04e535/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f66/8626842/5f43cf15c436/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f66/8626842/b002be5651bf/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f66/8626842/517c5b502da5/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f66/8626842/ed4e2b6189d3/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f66/8626842/89018346b78a/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f66/8626842/51d5fb04e535/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f66/8626842/5f43cf15c436/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f66/8626842/b002be5651bf/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f66/8626842/517c5b502da5/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f66/8626842/ed4e2b6189d3/gr6.jpg

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