Jin Yu, Shama Azi, Tang Haojinming, Zhao Ting, Zhang Xinyu, Yang Falong, Chen Dechun
College of Animal and Veterinary Sciences, Southwest Minzu University, Chengdu 610041, China.
Key Laboratory of Animal Medicine in Sichuan Province, Southwest Minzu University, Chengdu 610041, China.
Metabolites. 2025 May 14;15(5):326. doi: 10.3390/metabo15050326.
Ammonia (NH), a harmful gas, reduces livestock productivity, threatens their health, and causes economic losses. Luteolin (Lut), an anti-inflammatory flavonoid, may counteract these effects.
Our study explored luteolin's protective mechanisms on chicken splenic lymphocytes under ammonia stress using a simulation model and four-dimensional fast data-independent acquisition (4D-FastDIA) proteomics. We identified 316 proteins, with 69 related to ammonia's negative effects and 247 to Lut's protection. Thirty differentially expressed proteins (DEPs) were common to both groups, with 27 showing counter-regulation with Lut.
Gene Ontology (GO) analysis showed DEPs enriched in molecular responses to interferons and the negative regulation of immune responses, mainly located extracellularly. Molecular function analysis revealed DEPs in antigen binding and synthase activity. Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis linked DEPs to pathways like estrogen signaling, NOD-like receptor signaling, cytokine-cytokine receptor interaction, and JAK-STAT signaling. The quantitative real-time polymerase chain reaction (qRT-PCR) results indicated that the mRNA levels of Interferon Alpha and Beta Receptor subunit 2 (IFNAR2) and Signal Transducer and Activator of Transcription 1 (STAT1) were trending downward. This observation was in strong agreement with the downregulation noted in the proteomics analysis.
Lut's protective role against ammonia's adverse effects on chicken splenic lymphocytes is linked to the modulation of key signaling pathways, offering insights for further research on treating ammonia exposure with Lut.
氨(NH)是一种有害气体,会降低家畜生产力,威胁其健康并造成经济损失。木犀草素(Lut)是一种抗炎类黄酮,可能会抵消这些影响。
我们的研究使用模拟模型和四维快速非数据依赖采集(4D-FastDIA)蛋白质组学,探索了木犀草素在氨应激下对鸡脾淋巴细胞的保护机制。我们鉴定出316种蛋白质,其中69种与氨的负面影响相关,247种与木犀草素的保护作用相关。两组共有30种差异表达蛋白(DEP),其中27种显示出与木犀草素的反向调节。
基因本体(GO)分析表明,DEP在对干扰素的分子反应和免疫反应的负调节中富集,主要位于细胞外。分子功能分析揭示了DEP在抗原结合和合成酶活性方面的作用。京都基因与基因组百科全书(KEGG)分析将DEP与雌激素信号通路、NOD样受体信号通路、细胞因子-细胞因子受体相互作用和JAK-STAT信号通路等联系起来。定量实时聚合酶链反应(qRT-PCR)结果表明,干扰素α和β受体亚基2(IFNAR2)以及信号转导和转录激活因子1(STAT1)的mRNA水平呈下降趋势。这一观察结果与蛋白质组学分析中发现的下调情况高度一致。
木犀草素对氨对鸡脾淋巴细胞的不利影响具有保护作用,这与关键信号通路的调节有关,为进一步研究用木犀草素治疗氨暴露提供了思路。