College of Veterinary Medicine, Northeast Agricultural University, Harbin, 150030, China.
Biometals. 2023 Feb;36(1):137-152. doi: 10.1007/s10534-022-00468-4. Epub 2022 Nov 25.
Selenium (Se) is an essential trace element for the body. Various organs of the body, including the intestine, are affected by its deficiency. Se deficiency can induce oxidative stress and inflammatory responses in the intestine. It can also increase intestinal permeability and decrease intestinal immune function in mammals. However, the detailed studies, conducted on the intestinal molecular mechanisms of Se deficiency-induced injury in poultry, are limited. This study explored the adverse effects of Se deficiency on intestinal permeability and its mechanism. A Se-deficient chicken model was established, and the morphological changes in the chicken duodenum tissues were observed using a light microscope and transmission electron microscope (TEM). Western blotting, qRT-PCR, and other methods were used to detect the expression levels of selenoproteins, oxidative stress indicators, inflammatory factors, tight junction (TJ) proteins, antimicrobial peptides, and other related indicators in intestinal tissues. The results showed that Se deficiency could decrease the expression levels of selenoproteins and antioxidant capacity, activate the nuclear factor kappa-B (NF-κB) pathway, cause inflammation, and decrease the expression levels of TJ proteins and antimicrobial peptides in the duodenum tissues. The study also demonstrated that Se deficiency could increase intestinal permeability and decrease antimicrobial peptides via reactive oxygen species (ROS)/NF-κB. This study provided a theoretical basis for the scientific prevention and control of Se deficiency in poultry. Se deficiency decreased the expression levels of selenoproteins and increased ROS levels to activate the NF-κB pathway, resulting in the production of pro-inflammatory cytokines, reducing the expression levels of TJ protein, and weakening the expression of antimicrobial peptides, which contributed to the higher intestinal permeability. Oxidative stress weakened the expression of antimicrobial peptides.
硒(Se)是人体必需的微量元素。身体的各个器官,包括肠道,都会受到其缺乏的影响。硒缺乏会在肠道中引起氧化应激和炎症反应。它还可以增加哺乳动物的肠道通透性并降低肠道免疫功能。然而,关于硒缺乏诱导家禽肠道损伤的肠道分子机制的详细研究还很有限。本研究探讨了硒缺乏对肠道通透性的不良影响及其机制。建立了硒缺乏鸡模型,并用光学显微镜和透射电子显微镜(TEM)观察鸡十二指肠组织的形态变化。采用 Western blot、qRT-PCR 等方法检测肠道组织中硒蛋白、氧化应激指标、炎症因子、紧密连接(TJ)蛋白、抗菌肽等相关指标的表达水平。结果表明,硒缺乏可降低硒蛋白表达水平和抗氧化能力,激活核因子 kappa-B(NF-κB)途径,引起炎症,降低十二指肠组织中 TJ 蛋白和抗菌肽的表达水平。研究还表明,硒缺乏可通过活性氧物质(ROS)/NF-κB 增加肠道通透性并降低抗菌肽。本研究为科学防治家禽硒缺乏提供了理论依据。硒缺乏降低了硒蛋白的表达水平并增加了 ROS 水平以激活 NF-κB 途径,导致促炎细胞因子的产生,降低 TJ 蛋白的表达水平,并减弱抗菌肽的表达,从而导致更高的肠道通透性。氧化应激削弱了抗菌肽的表达。