Ammonia (NH3), a toxic gas, is an important cause of atmospheric haze and one of the main pollutants in air environment of poultry houses, threatening the health of human beings and poultry. However, little is known about the effect of NH3 on liver apoptotic damage. This study aimed to investigate the mechanism of oxidative stress-mediated apoptosis caused by NH3 in chicken livers and whether miR-187-5p/apaf-1 axis was involved in this mechanism. Here we duplicated NH3 poisoning model of chickens for fattening to study the ultrastructure of chicken livers, apoptosis rate, oxidative stress indexes, miR-187-5p, and apoptosis-related genes. Obvious apoptotic characteristics of liver tissues exposed to excess NH3 were observed, and the apoptosis rate increased. Excess NH3 decreased the activities of catalase (CAT), superoxide dismutase (SOD), total antioxidant capacity (T-AOC) and glutathione peroxidase (GSH-Px), and increased the content of malondialdehyde (MDA), suggesting that oxidative stress occurred. miR-187-5p decreased, and apoptotic protease activating factor-1 (apaf-1) increased, indicating that excess NH3 dysregulated miR-187-5p/apaf-1 axis. The expression of tumor protein p53 (p53), Bcl-2 associated X protein (Bax), Bcl-2 homologous antagonist/killer (Bak), Cytochrome-c (Cyt-c), Caspase-9, Caspase-8, and Caspase-3 was promoted, and the expression of B-cell lymphoma-2 (Bcl-2) was inhibited, resulting in apoptosis. Moreover, oxidative stress indexes, miR-187-5p, and apoptosis-related genes changed in dose- and time-dependent manner. Altogether, miR-187-5p/apaf-1 axis participated in oxidative stress-mediated apoptosis caused by NH3 via mitochondrial pathway in the livers of chickens for fattening. This study may provide new ideas to study the mechanism of liver apoptotic damage induced by NH3 exposure.

中文翻译：

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miR-187-5p / apaf-1轴参与了氧化应激介导的氨通过鸡肝线粒体途径引起的凋亡。

氨气（NH3）是造成大气雾霾的重要原因，也是禽舍空气环境中的主要污染物之一，威胁着人类和禽类的健康。然而，关于NH 3对肝细胞凋亡损伤的作用知之甚少。本研究旨在探讨NH3引起的氧化应激介导的鸡肝细胞凋亡的机制，以及miR-187-5p / apaf-1轴是否参与该机制。在这里，我们复制了用于繁殖的鸡的NH3中毒模型，以研究鸡肝的超微结构，细胞凋亡率，氧化应激指标，miR-187-5p和细胞凋亡相关基因。观察到暴露于过量NH 3的肝组织的明显凋亡特征，并且凋亡率增加。过量的NH3降低了过氧化氢酶（CAT），超氧化物歧化酶（SOD），总抗氧化能力（T-AOC）和谷胱甘肽过氧化物酶（GSH-Px），并增加了丙二醛（MDA）的含量，表明发生了氧化应激。miR-187-5p减少，而凋亡蛋白酶激活因子-1（apaf-1）增加，表明过量的NH3调节了miR-187-5p / apaf-1轴。肿瘤蛋白p53（p53），Bcl-2相关X蛋白（Bax），Bcl-2同源拮抗剂/杀手（Bak），细胞色素c（Cyt-c），Caspase-9，Caspase-8和Caspase的表达促进了-3，并且抑制了B细胞淋巴瘤2（Bcl-2）的表达，导致了细胞凋亡。而且，氧化应激指数，miR-187-5p和凋亡相关基因以剂量和时间依赖性方式改变。共，miR-187-5p / apaf-1轴通过线粒体途径参与雏鸡肝脏中由NH3引起的氧化应激介导的凋亡。该研究可能为研究NH3暴露引起的肝细胞凋亡损伤的机制提供新思路。