Hydrogen Sulfide Gas Exposure Induces Necroptosis and Promotes Inflammation through the MAPK/NF-κB Pathway in Broiler Spleen
Hydrogen Sulfide Gas Exposure Induces Necroptosis and Promotes Inflammation through the MAPK/NF-κB Pathway in Broiler Spleen
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DOI：
10.1155/2019/8061823
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发表时间：
2019-07-31
影响因子：
--
通讯作者：
Li, Shu
中科院分区：
文献类型：
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作者：
Chi, Qianru;Wang, Dongxu;Li, Shu
硫化氢（H2S）是大气中的主要污染物之一，严重威胁人类健康。鸡舍中含硫有机物的分解会产生大量的H2S，从而损害家禽健康。在本研究中，选择1日龄的肉鸡并暴露于4或20 ppm的H2S气体（0-3周：4 +/- 0.5 ppm，4-6周：20 +/- 0.5 ppm）。在第2、4和6周处死鸡后立即收集脾脏样品。组织病理学和超微结构观察显示，H2S暴露的脾脏具有明显的坏死特征。H2S暴露抑制GSH、CAT、T-AOC和SOD活性，增加NO、H2 O2、MDA含量和iNOS活性，诱导氧化应激。ATP酶活性和能量代谢相关基因的表达显著降低。此外，相关坏死性凋亡（RIPK 1、RIPK 3、MLKL、TAK 1、TAB 2和TAB 3）的表达显著增加，MAPK通路被激活。此外，H2S暴露激活了NF-κ B B经典途径，并诱导TNF-α和IL-1 β的释放。综上所述，我们得出结论，H2S暴露诱导氧化应激和能量代谢功能障碍;引起坏死性凋亡;激活MAPK通路，最终触发NF-κ B B通路;并促进鸡脾脏的炎症反应。
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-kappa B classical pathway and induced TNF-alpha and IL-1 beta 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-kappa B pathway; and promotes inflammatory response in chicken spleens.