Wang Le, Lu Houzhen, Gui Haitao, Ni Zifu, Sun Zhongke, Wang Zihua, Wang Zhihua, Liu Xuanyan, Yuan Qipeng
School of Biological Engineering, Institute of Biomass Science and Engineering, Henan University of Technology, 450001, Zhengzhou, China.
State Key Laboratory of Chemical Resource Engineering, Beijing University of Chemical Technology, 100029, Beijing, China.
Food Funct. 2025 Jul 1;16(13):5556-5572. doi: 10.1039/d4fo06475e.
Ulcerative colitis (UC) is a prevalent inflammatory bowel disease (IBD) posing a significant health threat. This study explored the protective effects of D-tagatose against DSS-induced colitis in mice and its underlying mechanisms using H&E staining, AB-PAS staining, immunofluorescence, immunohistochemistry, ELISA, qPCR, western blotting, and other assays. D-Tagatose improved colitis by increasing body weight and colon length, with decreased DAI (disease activity index) and histopathological scores. The results showed that D-tagatose inhibited the secretion of myeloperoxidase (MPO), inflammatory enzymes (iNOS and COX-2) and pro-inflammatory cytokines (TNF-α, IL-1β and IL-6) as well as increased the content of anti-inflammatory cytokines (IL-10) . In addition, D-tagatose enhanced the expression of tight junction proteins (ZO-1 and Occludin) and mucin (MUC-2). Furthermore, D-tagatose was able to modulate the gut microbiota dysbiosis caused by DSS-induced UC and increased the content of short-chain fatty acids (SCFAs). This study indicated that D-tagatose attenuated DSS-induced UC by modulating inflammatory cytokines, restoring intestinal barrier function, maintaining gut microbiota homeostasis, and enhancing SCFA production. These findings provide D-tagatose as a safe and effective novel functional food strategy for the prevention and treatment of UC.
溃疡性结肠炎（UC）是一种常见的炎症性肠病（IBD），对健康构成重大威胁。本研究利用苏木精-伊红染色、AB-PAS染色、免疫荧光、免疫组织化学、酶联免疫吸附测定、定量聚合酶链反应、蛋白质免疫印迹等检测方法，探讨了D-塔格糖对葡聚糖硫酸钠（DSS）诱导的小鼠结肠炎的保护作用及其潜在机制。D-塔格糖通过增加体重和结肠长度改善结肠炎，同时降低疾病活动指数（DAI）和组织病理学评分。结果表明，D-塔格糖抑制髓过氧化物酶（MPO）、炎症酶（诱导型一氧化氮合酶和环氧化酶-2）和促炎细胞因子（肿瘤坏死因子-α、白细胞介素-1β和白细胞介素-6）的分泌，并增加抗炎细胞因子（白细胞介素-10）的含量。此外，D-塔格糖增强紧密连接蛋白（闭合蛋白1和闭合蛋白）和黏蛋白（黏蛋白2）的表达。此外，D-塔格糖能够调节由DSS诱导的UC引起的肠道微生物群失调，并增加短链脂肪酸（SCFAs）的含量。本研究表明，D-塔格糖通过调节炎症细胞因子、恢复肠道屏障功能、维持肠道微生物群稳态和增强SCFA生成来减轻DSS诱导的UC。这些发现为D-塔格糖作为一种安全有效的新型功能性食品策略用于预防和治疗UC提供了依据。
