...
首页> 外文期刊>Biological trace element research >The Role of Nitric Oxide and Oxidative Stress in Intestinal Damage Induced by Selenium Deficiency in Chickens
【24h】

The Role of Nitric Oxide and Oxidative Stress in Intestinal Damage Induced by Selenium Deficiency in Chickens

机译:一氧化氮和氧化胁迫在鸡鸡缺乏症肠损伤中的作用

获取原文
获取原文并翻译 | 示例

摘要

Nitric oxide (NO) is an essential messenger molecule and is associated with inflammation and oxidative stress. Although NO has important biological functions in mammals, its role in the mechanism that occurs after intestinal injuries in chickens remains unknown. The objective of the present study was to investigate the real role of NO and oxidative stress in the intestinal injuries of chickens induced by selenium (Se) deficiency. A total 150 chickens were randomly divided into the following two groups: a low-Se group (L group, fed a Se-deficient diet containing 0.020 mg/kg Se) and a control group (C group, fed a commercial diet containing 0.2 mg/kg Se). The activities and mRNA levels of glutathione peroxidase (GSH-Px), the production of glutathione (GSH) and NO, and the protein and mRNA levels of inducible nitric oxide synthase (iNOS) were examined in the intestinal tissues (duodenum, jejunum, and rectum) at 15, 25, 35, 45, and 55 days. Methane dicarboxylic aldehyde (MDA) levels were also detected by assay kits. Then, the morphologies of the tissues were observed under the microscope after hematoxylin and eosin staining (H&E staining). The results showed that Se deficiency induced higher inflammatory damage and MDA levels (P < 0.05), which were accompanied by higher levels of iNOS and NO but lower levels of GSH and GSH-Px (P < 0.05). Our results indicated that Se deficiency induced oxidative damage in the intestinal tracts of chickens and that low levels of GSH-Px and high contents of NO may exert a major role in the injury of the intestinal tract induced by Se deficiency.
机译:一氧化氮(NO)是必需的信使分子,与炎症和氧化应激相关。虽然没有在哺乳动物中具有重要的生物学功能,但其在鸡鸡血损伤后的机制中的作用仍然未知。本研究的目的是研究NO和氧化应激在硒(SE)缺乏症诱导的鸡肠损伤中的真正作用。总150只鸡被随机分为以下两组:低Se组(L组,含有0.020mg / kg SE的SE缺乏饮食)和对照组(C组,喂养含0.2毫克的商业饮食/ kg se)。在肠组织中检查谷胱甘肽过氧化物酶(GSH-PX),谷胱甘肽(GSH)和NO的蛋白质和mRNA水平的活性和mRNA水平,以及诱导的一氧化氮合酶(INOS)的蛋白质和mRNA水平(Duodenum,Jejunum和直肠)在15,25,35,45和55天。通过测定试剂盒检测甲烷二羧酸醛(MDA)水平。然后,在苏木精和曙红染色(H&E染色)之后在显微镜下观察组织的形态。结果表明,SE缺乏诱导炎症损伤和MDA水平(P <0.05),伴随着较高水平的INOS和NO但下降的GSH和GSH-PX(P <0.05)。我们的研究结果表明,SE缺陷诱导鸡的肠道氧化损伤,并且低水平的GSH-PX和高含量的NO可能在SE缺乏症引起的肠道损伤中发挥重要作用。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号