Li Wangchang, Cao Duming, Shi Meiyi, Yang Xiaogan
Guangxi Key Laboratory of Animal Breeding, Disease Control and Prevention, College of Animal Science & Technology, Guangxi University, Nanning 530004, China.
Int J Mol Sci. 2025 Mar 24;26(7):2941. doi: 10.3390/ijms26072941.
Animals and humans are frequently infected by bacteria or exposed to bacterial derivatives in contaminated food, drinking water, or air, which significantly impacts their health. Among these bacterial sources, LPS (lipopolysaccharide) is the primary culprit. While it is widely known that LPS can cause liver inflammation and damage in animals, few studies have investigated this mechanism from the perspective of RNA editing. In this study, we administered LPS to mice via gavage to induce a liver injury model. We then used RNA editing omics approaches (RE-seq) to analyze RNA editing events potentially leading to liver inflammation following LPS administration, aiming to reveal the crucial role of RNA editing in LPS-induced processes. At the RNA editing level, we observed significant differences between the LPS group and the control (CON) group. Specifically, we identified 354 differentially edited genes, with 192 upregulated and 162 downregulated. These differentially edited genes were significantly enriched in pathways related to apoptosis, mTOR signaling, oxidative stress, and Nf-Kappa B signaling. By further integrating gene expression profiles and using a nine-quadrant analysis, we identified an important gene, , which showed significantly higher editing and expression levels in the LPS group. This gene is directly linked to liver inflammation and damage. The RNA editing of represents a significant potential mechanism underlying LPS-induced liver damage, providing a novel approach for addressing animal and human health issues.
动物和人类经常受到细菌感染，或在受污染的食物、饮用水或空气中接触细菌衍生物，这对它们的健康有重大影响。在这些细菌来源中，脂多糖（LPS）是主要元凶。虽然众所周知LPS会在动物体内引发肝脏炎症和损伤，但很少有研究从RNA编辑的角度研究这一机制。在本研究中，我们通过灌胃给小鼠施用LPS以诱导肝损伤模型。然后，我们使用RNA编辑组学方法（RE-seq）分析LPS给药后可能导致肝脏炎症的RNA编辑事件，旨在揭示RNA编辑在LPS诱导过程中的关键作用。在RNA编辑水平上，我们观察到LPS组和对照组（CON）之间存在显著差异。具体而言，我们鉴定出354个差异编辑基因，其中192个上调，162个下调。这些差异编辑基因在与细胞凋亡、mTOR信号传导、氧化应激和Nf-κB信号传导相关的途径中显著富集。通过进一步整合基因表达谱并使用九象限分析，我们鉴定出一个重要基因，该基因在LPS组中显示出显著更高的编辑和表达水平。该基因与肝脏炎症和损伤直接相关。[该基因名称未给出，此处无法准确翻译]的RNA编辑代表了LPS诱导肝损伤的一个重要潜在机制，为解决动物和人类健康问题提供了一种新方法。
