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The role of nitric oxide and autophagy in liver injuries induced by selenium deficiency in chickens

机译：一氧化氮和自噬在鸡氏症患者肝损伤中的作用

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摘要

Selenium (Se) is recognized as a necessary trace mineral in animal diets, including those of birds. Se deficiency induces a number of diseases and injuries in chickens, including liver damage. Nitric oxide (NO) is an essential messenger molecule associated with inflammation and oxidative stress. Autophagy is a cellular pathway that is crucial for development, differentiation, survival, and homeostasis, which maintain the balance of energy and nutrients for basic cell functions in the liver. However, little is known about the role of NO and autophagy in liver injured induced by Se deficiency. The aim of this study was to evaluate the influence of Se deficiency on NO and autophagy in chicken livers. A total of 300 1 day-old sea blue white laying hens were divided into two groups (n = 150 per group), and each of those groups was randomly divided into groups so that the trials were conducted in triplicate. The Se deficiency group (-Se) was fed a Se-deficient corn-soy basal diet (Se content 0.02 mg kg(-1)), and the Se-adequate group used as a control (+Se) was fed the same basal diet supplemented with Se at 0.2 mg kg(-1) (sodium selenite). The liver tissue was collected and examined for pathological observations, inducible NO synthase (iNOS)-NO activities (including NO content and iNOS activity), and mRNA and protein levels of autophagy genes at 15, 25, 35, 45, 55 and 65 days old. The results showed that numerous autophagosomes, as well as a low density of organelles and glycogen, were observed in the chicken livers from the Se deficiency group. In addition, the NO content and iNOS activity in the Se deficiency group were higher (P < 0.05) than in the control group. Transcript expression of autophagy genes (LC3-I, LC3-II, ATG5, Dynein and Beclin1) increased significantly (P < 0.05), and TOR gene expression fluctuated (first increased and then decreased) in the Se-deficient group compared with that in the corresponding control group. Meanwhile, the protein expression of autophagy genes (LC3-I, LC3-II, Dynein and Beclin1) also increased significantly (P < 0.05) in the Se-deficient group. This indicated that NO and autophagy are involved in the development of liver injury (pathological processes), which is induced by Se deficiency.
机译：硒（Se）是公认的动物饮食，包括那些鸟类的必要微量矿物质。硒缺乏诱导许多鸡疾病和损伤，包括肝损伤。一氧化氮（NO）是与炎症和氧化应激相关的一个重要信使分子。自噬是细胞途径就是发展，分化，存活和动态平衡，从而维持能量和营养素在肝细胞基本功能的平衡是至关重要的。然而，鲜为人知的是，NO的作用和自噬在肝脏中缺硒引起的受伤。这项研究的目的是评估硒缺乏对NO的鸡肝的影响和自噬。总共300 1日龄海蓝白色蛋鸡分为组（n = 150每组），并且每个这些基团的被随机分组​​，以使试验一式三份进行。硒缺乏组（-Se）送入一个缺硒玉米 - 大豆基础日粮（硒含量0.02毫克千克（-1）），和用作对照的硒足够组（+ Se）的进料相同的基础饮食补充有硒以0.2mg千克（-1）（亚硒酸钠）。肝组织收集并检查病理学观察，可诱导的NO合酶（iNOS）-NO活动（包括NO含量和iNOS活性），和mRNA且以15自噬基因的蛋白水平，25，35，45，55和65天老的。结果表明，大量的自噬体，以及细胞器和糖原的密度低，在从硒缺乏组鸡肝观察。此外，NO含量与iNOS活性的硒缺乏组中较高（P <0.05）低于对照组。自噬基因（LC3-I，LC3-II，ATG5，动力蛋白和Beclin1基因）的转录物表达显著增加（P <0.05），和TOR基因表达波动与在比较的硒缺乏组（先增大后减小）相应的对照组。同时，自噬基因（LC3-I，LC3-II，动力蛋白和Beclin1基因）的蛋白质表达也在硒缺乏组显著增加（P <0.05）。这表明，NO和自噬参与肝损伤（病理过程），这是由硒缺乏引起的发展。

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  • 来源
    《RSC Advances》 |2015年第62期|共8页
  • 作者

    Liu Chunpeng; Fu Jing; Liu Ci; Li Shu;

  • 作者单位

    Northeast Agr Univ Coll Vet Med Harbin 150030 Peoples R China;

    Northeast Agr Univ Coll Anim Sci &

    Technol Harbin 150030 Peoples R China;

    Northeast Agr Univ Coll Vet Med Harbin 150030 Peoples R China;

    Northeast Agr Univ Coll Vet Med Harbin 150030 Peoples R China;

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  • 正文语种 eng
  • 中图分类 化学;
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