Wang Hong-Tao, Weng Jia-Yi, Amadou Issoufou, Song Jie, Jiang Meng-Qi, Ci Wen-Jia, Zhu Jian-Jin
School of Food Science and Technology, Jiangnan University, Wuxi, 214122, Jiangsu, China; State Key Laboratory of Food Science and Resources, Jiangnan University, Wuxi, 214122, Jiangsu, China.
Laboratory of Food Science and Technology, Faculty of Agriculture and Environment Sciences, Dan Dicko Dankoulodo University of Maradi, Niger.
Microb Pathog. 2025 Aug;205:107670. doi: 10.1016/j.micpath.2025.107670. Epub 2025 May 8.
Inflammatory Bowel Disease (IBD) is a complex intestinal disorder that typically triggers inflammatory responses, immune dysregulation, and gut microbiota imbalance. Lignoformic acid (LFA) is a lignin-derived compound containing benzene rings and hydroxyl functional groups. It has antioxidant properties and can regulate intestinal pH. This study aimed to investigate the improve effects of LFA on dextran sulfate sodium (DSS)-induced chronic colitis in mice. The results showed that LFA treatment significantly improved body weight and Disease Activity Index (DAI) in mice and alleviated colon damage. In terms of oxidative stress and anti-inflammatory effects, the expression of antioxidant enzymes such as Glutathione Peroxidase (GSH-PX) and Superoxide Dismutase (SOD) was dose-dependently enhanced in DSS-induced mice. LFA reduced the expression of Tumor Necrosis Factor-alpha (TNF-α) by modulating the TLR4/MyD88/NF-κB signaling pathway. Furthermore, LFA dose-dependently increased the abundance of beneficial bacteria, including Akkermansia and Lachnospiraceae, and promoted the production of short-chain fatty acids (SCFAs). These findings suggest that LFA could serve as a therapeutic agent for colitis by enhancing intestinal barrier integrity, regulating inflammation, and restoring gut microbiota balance.
炎症性肠病（IBD）是一种复杂的肠道疾病，通常会引发炎症反应、免疫失调和肠道微生物群失衡。木质甲酸（LFA）是一种源自木质素的化合物，含有苯环和羟基官能团。它具有抗氧化特性，可调节肠道pH值。本研究旨在探讨LFA对葡聚糖硫酸钠（DSS）诱导的小鼠慢性结肠炎的改善作用。结果表明，LFA治疗显著改善了小鼠的体重和疾病活动指数（DAI），并减轻了结肠损伤。在氧化应激和抗炎作用方面，DSS诱导的小鼠中，谷胱甘肽过氧化物酶（GSH-PX）和超氧化物歧化酶（SOD）等抗氧化酶的表达呈剂量依赖性增强。LFA通过调节TLR4/MyD88/NF-κB信号通路降低肿瘤坏死因子-α（TNF-α）的表达。此外，LFA剂量依赖性地增加了有益细菌的丰度，包括阿克曼氏菌和毛螺菌科，并促进了短链脂肪酸（SCFAs）的产生。这些发现表明，LFA可通过增强肠道屏障完整性、调节炎症和恢复肠道微生物群平衡，作为治疗结肠炎的药物。
