首页> 外文期刊>Oxidative Medicine and Cellular Longevity >Hydrogen Sulfide Gas Exposure Induces Necroptosis and Promotes Inflammation through the MAPK/NF-κB Pathway in Broiler Spleen
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Hydrogen Sulfide Gas Exposure Induces Necroptosis and Promotes Inflammation through the MAPK/NF-κB Pathway in Broiler Spleen

机译:硫化氢气体曝光诱导肉体诱导肉鸡/ NF-κB途径的炎症

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摘要

Hydrogen sulfide (H2S) is one of the main pollutants in the atmosphere, which is a serious threat to human health. The decomposition of sulfur-containing organics in chicken houses could produce a large amount of H2S, thereby damaging poultry health. In this study, one-day-old broilers were selected and exposed to 4 or 20?ppm of H2S gas (0-3 weeks: 4±0.5?ppm, 4-6 weeks: 20±0.5?ppm). The spleen samples were collected immediately after the chickens were euthanized at 2, 4, and 6 weeks. The histopathological and ultrastructural observations showed obvious necrosis characteristics of H2S-exposed spleens. H2S exposure suppressed GSH, CAT, T-AOC, and SOD activities; increased NO, H2O2, and MDA content and iNOS activity; and induced oxidative stress. ATPase activities and the expressions of energy metabolism-related genes were significantly decreased. Also, the expressions of related necroptosis (RIPK1, RIPK3, MLKL, TAK1, TAB2, and TAB3) were significantly increased, and the MAPK pathway was activated. Besides, H2S exposure activated the NF-κB classical pathway and induced TNF-α and IL-1β release. Taken together, we conclude that H2S exposure induces oxidative stress and energy metabolism dysfunction; evokes necroptosis; activates the MAPK pathway, eventually triggering the NF-κB pathway; and promotes inflammatory response in chicken spleens.
机译:硫化氢(H2S)是大气中的主要污染物之一,这是对人类健康的严重威胁。鸡屋中含硫有机物的分解可以产生大量的H2S,从而损害家禽健康。在这项研究中,选择一天历史的肉鸡并暴露于4或20℃的H2S气体(0-3周:4±0.5〜5→PPM,4-6周:20±0.5?PPM)。在鸡在2,4,6周内将鸡被安乐死后立即收集脾样品。组织病理学和超微结构观察显示H2S暴露脾脏的明显坏死特性。 H2S暴露抑制了GSH,猫,T-AOC和SOD活动;不增加,H2O2和MDA含量和INOS活动;并诱导氧化应激。 ATP酶活性和能量代谢相关基因的表达显着降低。此外,相关死亡症(RIPK1,RIPK3,MLK1,TAK1,TAB2和TAB3)的表达显着增加,并且MAPK途径被激活。此外,H2S暴露激活NF-κB经典途径并诱导TNF-α和IL-1β释放。我们得出结论,H2S暴露会诱导氧化应激和能量代谢功能障碍;唤起虐疮;激活MAPK路径,最终触发NF-κB途径;并促进鸡脾脏的炎症反应。

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