Zeng Xianglin, Yin Lanmei, Zhang Yitong, Wang Qianqian, Li Jun, Yin Yuebang, Wang Qiye, Li Jianzhong, Yang Huansheng
Hunan International Joint Laboratory of Animal Intestinal Ecology and Health, Laboratory of Animal Nutrition and Human Health, College of Life Sciences, Hunan Normal University, Changsha, 410081, Hunan, China.
Hunan Provincial Key Laboratory of Animal Nutritional Physiology and Metabolic Process, Scientific Observing and Experimental Station of Animal Nutrition and Feed Science in South-Central, Ministry of Agriculture, Key Laboratory of Agro-Ecological Processes in Subtropical Region, Institute of Subtropical Agriculture, Hunan Provincial Engineering Research Center for Healthy Livestock and Poultry Production, Chinese Academy of Sciences, Changsha, 410125, Hunan, China.
Biol Trace Elem Res. 2025 Feb 25. doi: 10.1007/s12011-025-04546-9.
Iron deficiency is the most common comorbidity of inflammatory bowel disease (IBD), but the effect of iron supplementation on the repair processes of intestinal injury in weaned mice is unknown. This study aimed to evaluate the potential mechanism of dietary iron on intestinal injury and intestinal regeneration in the dextran sodium sulfate (DSS)-induced colitis of the weaned mouse model. The mice were fed either a control diet containing (45.00 mg/kg Fe) or iron supplemental (448.30 mg/kg Fe) diet for 14 days, followed by a 7-day oral administration of 2.5% DSS to all mice. The result showed that at day 0 of the recovery period (0 DRP), the impact of iron on the gut index and intestinal morphology was found to be more significant in weaned mice compared to adult mice. At 3 DRP, the iron diet alleviated inflammation-induced weight loss, shortening of colon length, thickening of the muscle layer, and disruption of gut morphology. At 0, 3, and 7 DRP, we found that an iron diet increased intestinal stem cell (ISC) viability and protected epithelial integrity. Furthermore, FeSO significantly enhanced organoid viability and increased mRNA expression of differentiation, ISC, and retinol metabolism-related marker genes in the organoids compared with the control group. Overall, this study demonstrates that the iron diet accelerates intestinal regeneration after intestinal injury in weaned mice by activating the retinol metabolic pathway to regulate the proliferation and differentiation of ISCs.
缺铁是炎症性肠病（IBD）最常见的合并症，但铁补充剂对断奶小鼠肠道损伤修复过程的影响尚不清楚。本研究旨在评估日粮铁对葡聚糖硫酸钠（DSS）诱导的断奶小鼠模型结肠炎中肠道损伤和肠道再生的潜在机制。将小鼠喂食含（45.00mg/kg铁）的对照日粮或铁补充（448.30mg/kg铁）日粮14天，然后对所有小鼠口服2.5% DSS 7天。结果显示，在恢复期第0天（0 DRP），与成年小鼠相比，铁对断奶小鼠肠道指数和肠道形态的影响更为显著。在3 DRP时，铁日粮减轻了炎症引起的体重减轻、结肠长度缩短、肌层增厚和肠道形态破坏。在0、3和7 DRP时，我们发现铁日粮增加了肠道干细胞（ISC）活力并保护了上皮完整性。此外，与对照组相比，硫酸亚铁显著提高了类器官活力，并增加了类器官中分化、ISC和视黄醇代谢相关标记基因的mRNA表达。总体而言，本研究表明，铁日粮通过激活视黄醇代谢途径来调节ISC的增殖和分化，从而加速断奶小鼠肠道损伤后的肠道再生。
