Ulcerative colitis (UC) is a complex, multifactorial disorder which can be aggravated by oxidative stress. Dextran sulfate sodium (DSS)-induced UC in inbred mice is the most commonly used animal-model. However, these populations lack genetic variability therefore this study aimed to establish a DSS-induced UC model in outbred ICR mice and to assess its association with the oxidant-antioxidant system. Male ICR mice were administered a 40 kDa-DSS solution (6 g/kg/day; 0.25 mL 21% DSS 4 times per day) intragastrically for 4 and 7 consecutive days (n = 5). Disease activity index (DAI) was determined daily from body weight and stool characteristics. At the end of the study, colons were collected to examine histology, myeloperoxidase activity, and expression of superoxide dismutase 1 and 2 (Sod1 and Sod2) and catalase (Cat). DSS-treated mice demonstrated daily increases in DAI score with significantly shortened colons, an indirect marker of inflammation in UC. Histological examination of DSS-treated colons revealed goblet cell loss, crypt damage, and epithelial erosion, followed by infiltration of mast cells to the mucosa with mucin depletion. Myeloperoxidase activity was elevated in the DSS-treated mice while Sod1, Sod2, and Cat were suppressed compared to controls. A DSS-induced UC model was established in ICR mice with associated oxidative stress triggering. This outbred-mouse model could prove useful for investigating the underlying pathophysiological mechanisms of UC in terms of oxidant-antioxidant balance.

溃疡性结肠炎（UC）是一种复杂的多因素疾病，可因氧化应激而加剧。硫酸葡聚糖硫酸钠（DSS）诱导的近交小鼠的UC是最常用的动物模型。但是，这些种群缺乏遗传变异性，因此，本研究旨在在远距离ICR小鼠中建立DSS诱导的UC模型，并评估其与氧化剂-抗氧化剂系统的关系。雄性ICR小鼠在胃内连续4天和7天被给予40kDa-DSS溶液（6g / kg /天； 0.25mL 21％DSS，每天4次）。每天根据体重和粪便特征确定疾病活动指数（DAI）。在研究结束时，收集结肠以检查组织学，髓过氧化物酶活性以及超氧化物歧化酶1和2（Sod1和Sod2）和过氧化氢酶（Cat）。经DSS处理的小鼠表现出DAI评分的每日增加，结肠明显缩短，结肠是UC炎症的间接标志。经DSS处理的结肠的组织学检查显示杯状细胞丢失，隐窝损伤和上皮侵蚀，随后肥大细胞浸润至粘膜，同时粘液消耗。与对照组相比，DSS处理的小鼠中的髓过氧化物酶活性升高，而Sod1，Sod2和Cat受到抑制。在ICR小鼠中建立了DSS诱导的UC模型，并伴有相关的氧化应激触发。该杂种小鼠模型可能被证明可用于研究氧化剂的抗氧化剂平衡的潜在的UC病理生理机制。