Xiong Yanling, Cheng Zhentao, Zhang Yangzi, Liu Ting, Wan Zhiling, Xia Cuiyun, Zhou Binlan, Shan Chunlan, Song Derong, Miao Fujun
College of Animal Science, Guizhou University, Guiyang, 550000, People's Republic of China.
Guizhou Academy of Agricultural Sciences, Guiyang, 550001, People's Republic of China.
Eur J Nutr. 2025 Jan 7;64(1):64. doi: 10.1007/s00394-024-03577-7.
Ulcerative colitis (UC) can cause severe oxidative stress in the colon, which can lead to tissue damage and an imbalance in the normal gut microbiota. Ellagic acid (EA) is one of the main types of plant polyphenols with improved pharmacological effects such as antioxidant, anti-inflammatory, and antibacterial properties. However, currently, the studies on the impact of EA on the gut microbiota and its potential to alleviate UC in mice through the ROS/NLRP3 pathway are limited. In this study, dextran sodium sulfate (DSS) was used to construct a UC mouse model, which was then treated with EA as an intervention for UC. The results revealed that EA alleviated the trend of liver, spleen, and weight changes in UC mice and improved colon oxidative stress, inflammation, and pathological damage. Mechanistically, DSS-induced UC indicated a significant increase in ROS/NLRP3 pathway-related factors, whereas EA intervention activated the Nrf2 pathway to reduce these factors. Furthermore, the DSS group had a reduced abundance of Firmicutes (59.02%) and an increased abundance of Bacteroides and Proteobacterium by 1.8 times and 10.16%; however, EA intervention reversed these changes, thus alleviating UC. The findings of this study revealed that EA could significantly enhance the composition of gut microbiota in UC and reduce the inflammatory response, colonic damage as well as oxidative stress caused by DSS by regulating the ROS/NLRP3 pathway. These results provide novel perspectives on the prevention and treatment strategies of UC and highlight the therapeutic benefits of EA in managing colitis.
溃疡性结肠炎（UC）可在结肠中引发严重的氧化应激，进而导致组织损伤以及正常肠道微生物群失衡。鞣花酸（EA）是植物多酚的主要类型之一，具有抗氧化、抗炎和抗菌等多种药理作用。然而，目前关于EA对肠道微生物群的影响及其通过ROS/NLRP3途径缓解小鼠UC的潜力的研究有限。在本研究中，使用葡聚糖硫酸钠（DSS）构建UC小鼠模型，然后用EA作为UC的干预措施进行治疗。结果显示，EA缓解了UC小鼠肝脏、脾脏和体重变化的趋势，并改善了结肠的氧化应激、炎症和病理损伤。从机制上讲，DSS诱导的UC表明ROS/NLRP3途径相关因子显著增加，而EA干预激活了Nrf2途径以减少这些因子。此外，DSS组厚壁菌门丰度降低（59.02%），拟杆菌门和变形菌门丰度分别增加1.8倍和10.16%；然而，EA干预逆转了这些变化，从而缓解了UC。本研究结果表明，EA可通过调节ROS/NLRP3途径显著改善UC小鼠肠道微生物群的组成，并减轻DSS引起的炎症反应、结肠损伤和氧化应激。这些结果为UC的预防和治疗策略提供了新的视角，并突出了EA在治疗结肠炎方面的益处。
