分子与细胞营养 MOLECULAR AND CELLULAR NUTRITION

黑沙蒿多糖对脂多糖刺激的免疫应激肉仔鸡十二指肠中免疫指标及相关基因和蛋白表达的影响

  • 邢媛媛 ,
  • 郑彦楷 ,
  • 郭世伟 ,
  • 王俊丽 ,
  • 金晓 ,
  • 徐元庆 ,
  • 史彬林
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  • 内蒙古农业大学动物科学学院, 呼和浩特 010018
邢媛媛(1991-),女,内蒙古丰镇人,博士研究生,研究方向为动物环境与营养。E-mail:xingyuanyuan2014@163.com

收稿日期: 2020-12-20

  网络出版日期: 2021-07-06

基金资助

国家自然科学基金项目(31960667)

Effects of Artemisia ordosica Polysaccharide on Immune Indexes and Expression of Related Genes and Proteins in Duodenum of Immune-Stressed Broilers Challenged by Lipopolysaccharide

  • XING Yuanyuan ,
  • ZHENG Yankai ,
  • GUO Shiwei ,
  • WANG Junli ,
  • JIN Xiao ,
  • XU Yuanqing ,
  • SHI Binlin
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  • College of Animal Science, Inner Mongolia Agricultural University, Hohhot 010018, China

Received date: 2020-12-20

  Online published: 2021-07-06

Supported by

 

摘要

本试验旨在探讨黑沙蒿多糖(AOP)对脂多糖(LPS)刺激的免疫应激肉仔鸡十二指肠炎症的缓解作用及其可能的作用机制。试验选取192只1日龄爱拔益加(AA)肉仔鸡,随机分为4个处理,每个处理6个重复,每个重复8只鸡。试验期为42 d,分为预试期(第1~14天)、应激Ⅰ期(第15~28天,包括7 d的LPS注射期和7 d的恢复期)和应激Ⅱ期(第29~42天,包括7 d的LPS注射期和7 d的恢复期)。处理1和2饲喂基础饲粮,处理3和4饲喂试验饲粮(在基础饲粮中添加750 mg/kg AOP)。分别在应激Ⅰ期(试验第15、17、19、21天)和应激Ⅱ期(试验第29、31、33、35天)给处理1和3的肉仔鸡腹腔注射LPS溶液,处理2和4注射等量的生理盐水。在第21和35天,每个重复随机选取1只鸡,屠宰后迅速取十二指肠组织样品,用于测定免疫指标及其相关基因和蛋白表达量。结果表明:饲粮中添加AOP显著缓解了由LPS导致的肉仔鸡生长性能的下降;此外,饲粮添加AOP显著缓解了由LPS导致的肉仔鸡十二指肠中白细胞介素(IL)-1β(第21和35天)、IL-6(第21和35天)和IL-4(第21天)的过度产生(P<0.05),且显著缓解了十二指肠中免疫球蛋白M(IgM,第21天)含量的过度下降(P<0.05);同时,饲粮添加AOP显著缓解了由LPS导致的肉仔鸡十二指肠中核转录因子-κB p65(NF-κB p65)(第35天)和IL-1β(第21天)基因以及NF-κB信号通路相关蛋白(NF-κB p65、IL-1β和IL-6,第21和35天)的过表达(P<0.05),且显著促进了核转录因子-κB的抑制物α(IκBα)(第21和35天)的蛋白表达(P<0.05)。由此推测,AOP可通过抑制NF-κB信号通路的过度激活来缓解LPS导致的肉仔鸡十二指肠中促炎因子的过度释放。

本文引用格式

邢媛媛 , 郑彦楷 , 郭世伟 , 王俊丽 , 金晓 , 徐元庆 , 史彬林 . 黑沙蒿多糖对脂多糖刺激的免疫应激肉仔鸡十二指肠中免疫指标及相关基因和蛋白表达的影响[J]. 动物营养学报, 2021 , 33(7) : 4068 -4078 . DOI: 10.3969/j.issn.1006-267x.2021.07.048

Abstract

This experiment investigated the mitigative effect of Artemisia ordosica polysaccharide (AOP) on duodenal inflammation of immune-stressed broilers challenged by lipopolysaccharide (LPS) and its possible mechanism. A total of 192 one-day-old Arbor Acres (AA) broilers were randomly allotted to four treatments with 6 replicates and each replicate had 8 broilers. The experiment lasted for 42 d, and it included preliminary phase (days 1 to 14), stress periods Ⅰ (days 15 to 28, including 7 d of injection period and 7 d of convalescent period), and stress period Ⅱ (days 28 to 42, including 7 d of injection period and 7 d of convalescent period). Broilers in treatments 1 and 2 were fed a basal diet, and those in treatments 3 and 4 were fed an experiment diet (supplemented with 750 mg/kg AOP in the basal diet). During stress periods Ⅰ (days 15, 17, 19 and 21 of experiment) and Ⅱ (days 29, 31, 33 and 35 of experiment), broilers in treatments 1 and 3 were injected intra-abdominally with LPS solution, and those in treatments 2 and 4 were injected intra-abdominally with equal amount of sterile saline. At days 21 and 35, one broiler from each replicate was slaughtered to collect duodenum tissue, which was used to measure the immune indexes and the expression levels of related genes and proteins. The results showed that AOP supplementation significantly alleviated the decrease of growth performance induced by LPS (P<0.05). AOP supplementation significantly alleviated the overproduction of interleukin (IL)-1β (days 21 and 35), IL-6 (days 21 and 35) and IL-4 (day 21) in duodenum of broilers induced by LPS (P<0.05), and significantly alleviated the excessive decline of immunoglobulin M (IgM) content (day 21) in duodenum (P<0.05). Additionally, AOP supplementation significantly alleviated the over-expression of nuclear factor-κB p65 (NF-κB p65) (day 35) and IL-1β (day 21) genes in duodenum of broilers induced by LPS (P<0.05), as well as the nuclear factor-κB (NF-κB) signaling pathway related proteins (NF-κB p65, IL-1β and IL-6, days 21 and 35) (P<0.05), and significantly promoted the protein expression of NF-κB inhibitor α (IκBα) (P<0.05). Collectively, AOP can alleviate the excessive release of proinflammatory factors in duodenum of broilers induced by LPS by inhibiting the excessive activation of NF-κB signaling pathway.

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