Introduction to UC Animal Models

Ulcerative colitis (UC) animal models are classic experimental systems used to mimic human chronic inflammatory bowel disease. They are primarily established through chemical induction, such as the dextran sulfate sodium (DSS)-in‑drinking‑water method and the 2,4,6‑trinitrobenzenesulfonic acid (TNBS) enema technique. Following model establishment, these approaches can induce disruption of the colonic mucosal barrier, epithelial injury, and extensive infiltration of inflammatory cells, resulting in hallmark clinical manifestations including diarrhea, hematochezia, weight loss, and colonic shortening. Concurrently, they are associated with elevated levels of pro‑inflammatory cytokines such as TNF‑α and IL‑6, as well as impaired intestinal barrier function. This model is widely employed for investigating the pathogenic mechanisms of inflammatory bowel disease and for in vivo evaluation of anti‑inflammatory and gut‑repair–targeted therapeutics.

Advantages of Aniphe BioLab’s UC Animal Model Platform Services

The Aniphe BioLab ulcerative colitis (UC) animal model platform is centered on its ability to stably induce intestinal inflammation and reproducibly disrupt the colonic barrier, providing a reliable in vivo model system for studying the mechanisms of inflammatory bowel disease and evaluating gut‑repair therapeutics.

	Multiple modeling approaches are well-established. It supports the establishment of classic UC models, such as DSS‑induced drinking water–based and TNBS‑induced enema models, and is adaptable to the needs of different research stages.
	Inflammation-induced stability and controllability By precisely modulating the dose and induction cycle, we can systematically establish graded models of colitis spanning mild, moderate, and severe phenotypes.
	The model exhibits high reproducibility. Standardized dosing and feeding protocols reduce individual variability and enhance batch-to-batch consistency.
	Complete clinical indicators It can reliably induce typical UC manifestations, including weight loss, diarrhea, hematochezia, and colonic shortening.
	The multi-dimensional evaluation system has been refined. Systematic assessment is achieved by integrating DAI scores, histopathological findings, and inflammatory cytokine measurements.

Modeling cycle	1–3 weeks
Laboratory animals	Mice and rats of SPF grade
Positive drug	Sulfasalazine or 5-aminosalicylic acid (5-ASA, a topical anti-inflammatory), dexamethasone (a glucocorticoid), infliximab (an anti-TNF‑α monoclonal antibody), cyclosporine A (a calcineurin inhibitor), and others.
Application areas	Pathogenesis of UC (intestinal barrier dysfunction, dysbiosis, and immune dysregulation); screening of anti-inflammatory and mucosal‑healing agents; evaluation of the efficacy of biologics and JAK inhibitors; research on the gut–brain axis, probiotics, and fecal microbiota transplantation strategies.

Construction of UC Animal Models

The DSS‑induced model involves adding dextran sulfate sodium (DSS) to the drinking water, which disrupts the intestinal epithelial barrier, activates innate immunity, and triggers an acute colitis response characterized by diarrhea, hematochezia, and weight loss. In contrast, the TNBS‑ethanol enema model first damages the intestinal mucosal barrier with ethanol and then administers TNBS, allowing it to bind to intestinal proteins and form antigens that elicit a T‑cell‑mediated delayed‑type hypersensitivity reaction, thereby inducing marked intestinal wall inflammation and ulceration. The adoptive T‑cell transfer model, on the other hand, induces chronic, immune‑mediated colitis by transferring pathogenic CD4⁺ T cells into immunocompromised mice, thus more closely mimicking the immune pathogenesis of human chronic ulcerative colitis.

The three models respectively encompass the distinct pathological stages of acute inflammation, chemical injury, and immune dysregulation, making them crucial experimental platforms for investigating the mechanisms of inflammatory bowel disease and evaluating pharmacological interventions.