Effect of Hydrogen-rich Water on Chronic Kappa-carrageenan-induced Colitis in Weaned Female Swiss Albino Mice: A Preliminary Study

阿克曼西亚 断奶 医学 生理学 肠道菌群 某种肠道细菌 免疫系统 双歧杆菌 免疫学 炎症性肠病 促炎细胞因子 结肠炎 疾病 白细胞介素10 胃肠病学 细胞因子 抗氧化剂 益生菌 相伴的 腹泻 粪便 小肠结肠炎 内科学 炎症 免疫 体重 生物
作者
Oumaima Anachad,Wafaa Taha,Hicham Wahnou,Imad Fenjar,Mohamed Rida Salam,Hasnae Zekhnini,Houssam Assoui,Amina Kardoudi,Abdelouaheb Benani,Faïza Bennis,Fatima Chegdani
出处
期刊:Recent advances in inflammation & allergy drug discovery [Bentham Science]
卷期号:20
标识
DOI:10.2174/0127722708469109260622071700
摘要

INTRODUCTION: Food additives such as carrageenan, which are widely present in processed foods, can aggravate intestinal inflammation, particularly during the weaning period, a stage of high gut vulnerability. Weaned mice provide a relevant model to study how early dietary exposures influence intestinal health. This preliminary study explores the potential applicability of Hydrogen-rich Water (HRW), a non-pharmacological approach with antioxidant and anti-inflammatory properties, as an early-stage and potentially patentable supportive strategy against carrageenan-induced colitis. METHODS: Weaned female Swiss albino mice were assigned to four groups: normal control, UC, HRW, and diclofenac. Except for controls, all groups were exposed to kappa-carrageenan in drinking water for three months to induce chronic colitis, followed by a two-week treatment with HRW or diclofenac. Clinical signs, colon length, histopathology, cytokine expression, and gut microbiota composition were analyzed. RESULTS: Carrageenan exposure in weaned mice caused significant colitis, evidenced by body weight loss, an increase in disease activity index, colon shortening, and severe inflammatory lesions. Pro-inflammatory cytokines TNF-α, IL1β, and IL6 were significantly upregulated with a concomitant decrease in IL10. HRW treatment significantly attenuated disease severity by reducing disease activity index, preserving colon length, decreasing pro-inflammatory cytokines, and partially restoring IL10 expression. However, HRW had limited effects on the relative abundance of beneficial gut microbes such as Bifidobacterium spp. and Akkermansia spp. DISCUSSION: These preliminary findings support existing evidence that early-life exposure to food additives disrupts immune regulation in the immature gut. The protective effects of HRW appear to be mainly host-mediated, suggesting an innovative but early-stage immunomodulatory mechanism rather than a microbiota-driven effect. CONCLUSION: Overall, this exploratory proof-of-concept study suggests that HRW may represent a promising and potentially patentable supportive approach for reducing diet-induced intestinal inflammation during weaning. Further validation is required before any translational or industrial application can be considered.

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