Gallic Acid Ameliorated Chronic DSS‐Induced Colitis Through Gut Microbiota Modulation, Intestinal Barrier Improvement, and Inflammation

IF 4.2 2区 农林科学 Q1 FOOD SCIENCE & TECHNOLOGY Molecular Nutrition & Food Research Pub Date : 2025-03-24 DOI:10.1002/mnfr.70024
Baoming Tian, Peng Ye, Xue Zhou, Jiangning Hu, Peiyi Wang, Ming Cai, Kai Yang, Peilong Sun, Xianguo Zou
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Abstract

Scope: Gallic acid (GA) is recognized for its purported antiinflammatory properties. GA has been demonstrated to prevent and alleviate the symptoms of chronic colitis through the modulation of the gut microbiota, improvement of the intestinal barrier, and reduction of inflammation.Methods and results: In order to determine the mechanism by which GA exerts its protective effect against chronic colitis, mice were induced by dextran sulfate sodium (DSS). The reduction in the disease activity index by 25% and the decrease in colon tissue damage indicated that 36 days of GA intervention alleviated chronic DSS‐induced colitis symptoms. GA was observed to mitigate weight loss by 2.5% and the shortening of colon by 17.3%, and to diminish the expression of pivotal proteins within the TLR4/nuclear factor κB (NF‐κB) signaling cascades, consequently lowering the generation of inflammatory cytokines. Furthermore, GA effectively corrected the gut microbiota imbalance, increased the content of short‐chain fatty acids (SCFAs), which in turn suppressed inflammation, and enhanced tight junction protein expression, thereby strengthening the intestinal barrier. Conclusion: GA has the capacity to enhance the efficacy of chronic colitis through a multifaceted mechanism, influencing the gut microbiota, intestinal barrier function, and inflammatory processes. The findings highlight the potential of GA as a preventative strategy for chronic colitis.
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没食子酸通过调节肠道菌群、改善肠道屏障和炎症改善慢性DSS诱导的结肠炎
范围:没食子酸(GA)被认为具有抗炎特性。GA已被证明可以通过调节肠道菌群、改善肠道屏障和减少炎症来预防和减轻慢性结肠炎的症状。方法与结果:为探讨GA对慢性结肠炎的保护作用机制,采用葡聚糖硫酸钠(DSS)诱导小鼠进行实验。疾病活动指数降低25%,结肠组织损伤减少,表明36天的GA干预缓解了慢性DSS诱导的结肠炎症状。研究发现,GA可使体重减轻2.5%,结肠缩短17.3%,并减少TLR4/核因子κB (NF‐κB)信号级联中关键蛋白的表达,从而降低炎症细胞因子的产生。此外,GA有效地纠正了肠道菌群失衡,增加了短链脂肪酸(SCFAs)的含量,从而抑制了炎症,并增强了紧密连接蛋白的表达,从而加强了肠道屏障。结论:GA可通过多种机制提高慢性结肠炎的疗效,影响肠道菌群、肠道屏障功能和炎症过程。研究结果强调了GA作为慢性结肠炎预防策略的潜力。
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来源期刊
Molecular Nutrition & Food Research
Molecular Nutrition & Food Research 工程技术-食品科技
CiteScore
8.70
自引率
1.90%
发文量
250
审稿时长
1.7 months
期刊介绍: Molecular Nutrition & Food Research is a primary research journal devoted to health, safety and all aspects of molecular nutrition such as nutritional biochemistry, nutrigenomics and metabolomics aiming to link the information arising from related disciplines: Bioactivity: Nutritional and medical effects of food constituents including bioavailability and kinetics. Immunology: Understanding the interactions of food and the immune system. Microbiology: Food spoilage, food pathogens, chemical and physical approaches of fermented foods and novel microbial processes. Chemistry: Isolation and analysis of bioactive food ingredients while considering environmental aspects.
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