ScopeThis study investigates the potential of glutamine to mitigate intestinal mucositis and dysbiosis caused by the chemotherapeutic agent 5‐fluorouracil (5‐FU).Methods and resultsOver twelve days, Institute of Cancer Research (ICR) mice are given low (0.5 mg kg−1) or high (2 mg kg−1) doses of L‐Glutamine daily, with 5‐FU (50 mg kg−1) administered between days six and nine. Mice receiving only 5‐FU exhibited weight loss, diarrhea, abnormal cell growth, and colonic inflammation, correlated with decreased mucin proteins, increased endotoxins, reduced fecal short‐chain fatty acids, and altered gut microbiota. Glutamine supplementation counteracted these effects by inhibiting the Toll‐like receptor 4/nuclear factor kappa B (TLR4/NF‐κB) pathway, modulating nuclear factor erythroid 2‐related factor 2/heme oxygenase 1 (Nrf2/HO‐1) oxidative stress proteins, and increasing mammalian target of rapamycin (mTOR) levels, thereby enhancing microbial diversity and protecting intestinal mucosa.ConclusionsThese findings underscore glutamine's potential in preventing 5‐FU‐induced mucositis by modulating gut microbiota and inflammation pathways.

中文翻译：

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L-谷氨酰胺通过调节肠道微生物群和维持小鼠肠道屏障的完整性，显着改善 5-氟尿嘧啶引起的肠粘膜炎

范围本研究调查了谷氨酰胺减轻化疗药物 5-氟尿嘧啶 (5-FU) 引起的肠道粘膜炎和生态失调的潜力。方法和结果在 12 天的时间里，癌症研究所 (ICR) 小鼠接受低剂量（0.5 mg/kg）注射−1）或高（2 mg kg−1）每日 L-谷氨酰胺剂量，含 5-FU（50 mg/kg−1）在第六天和第九天之间进行。仅接受 5-FU 的小鼠表现出体重减轻、腹泻、细胞生长异常和结肠炎症，与粘蛋白蛋白减少、内毒素增加、粪便短链脂肪酸减少和肠道微生物群改变相关。谷氨酰胺补充剂通过抑制 Toll 样受体 4/核因子 kappa B (TLR4/NF-κB) 通路、调节核因子红细胞 2 相关因子 2/血红素加氧酶 1 (Nrf2/HO-1) 氧化应激蛋白来抵消这些影响，并增加哺乳动物雷帕霉素靶点 (mTOR) 水平，从而增强微生物多样性并保护肠粘膜。结论这些发现强调了谷氨酰胺通过调节肠道微生物群和炎症途径预防 5-FU 诱导的粘膜炎的潜力。