Chen Yongjie, Zhang Runxiang, Ding Susu, Nian Haoyang, Zeng Xiangyin, Liu Honggui, Xing Houjuan, Li Jianhong, Bao Jun, Li Xiang
College of Animal Science and Technology, Northeast Agricultural University, Harbin 150030, China.
Key Laboratory of Swine Facilities, Ministry of Agriculture, Northeast Agricultural University, Changjiang Road No. 600, Harbin 150030, China.
Animals (Basel). 2022 May 7;12(9):1204. doi: 10.3390/ani12091204.
Ammonia is one of the major environmental pollutants that seriously threaten human health. Although many studies have shown that ammonia causes oxidative stress and inflammation in spleen tissue, the mechanism of action is still unclear. In this study, the ammonia poisoning model of fattening pigs was successfully established. We examined the morphological changes and antioxidant functions of fattening pig spleen after 30-day exposure to ammonia. Effects of ammonia in the fattening pig spleen were analyzed from the perspective of oxidative stress, inflammation, and histone methylation via transcriptome sequencing technology (RNA-seq) and real-time quantitative PCR validation (qRT-PCR). We obtained 340 differential expression genes (DEGs) by RNA-seq. Compared with the control group, 244 genes were significantly upregulated, and 96 genes were significantly downregulated in the ammonia gas group. Some genes in Gene Ontology (GO) terms were verified and showed significant differences by qRT-PCR. The KEGG pathway revealed significant changes in the MAPK signaling pathway, which is strongly associated with inflammatory injury. To sum up, the results indicated that ammonia induces oxidative stress in pig spleen, activates the MAPK signaling pathway, and causes spleen necrosis and injury. In addition, some differential genes encoding epigenetic factors were found, which may be involved in the response mechanism of spleen tissue oxidative damage. The present study provides a transcriptome database of ammonia-induced spleen poisoning, providing a reference for risk assessment and comparative medicine of ammonia.
氨是严重威胁人类健康的主要环境污染物之一。尽管许多研究表明氨会导致脾脏组织的氧化应激和炎症，但作用机制仍不清楚。在本研究中，成功建立了育肥猪氨中毒模型。我们检测了育肥猪脾脏在暴露于氨30天后的形态变化和抗氧化功能。通过转录组测序技术（RNA-seq）和实时定量PCR验证（qRT-PCR），从氧化应激、炎症和组蛋白甲基化的角度分析了氨对育肥猪脾脏的影响。通过RNA-seq我们获得了340个差异表达基因（DEG）。与对照组相比，氨气组中有244个基因显著上调，96个基因显著下调。基因本体论（GO）术语中的一些基因通过qRT-PCR得到验证并显示出显著差异。KEGG通路显示丝裂原活化蛋白激酶（MAPK）信号通路有显著变化，这与炎症损伤密切相关。综上所述，结果表明氨诱导猪脾脏氧化应激，激活MAPK信号通路，导致脾脏坏死和损伤。此外，还发现了一些编码表观遗传因子的差异基因，它们可能参与脾脏组织氧化损伤的反应机制。本研究提供了氨诱导脾脏中毒的转录组数据库，为氨的风险评估和比较医学提供了参考。
