TNBS-Induced Ulcerative Colitis Model

Model Introduction

The TNBS (2,4,6-Trinitrobenzenesulfonic acid)-induced Ulcerative Colitis (UC) model is a classic model for studying immune-mediated organ injury. The principle is that TNBS acts as a hapten and enters intestinal tissue with the aid of ethanol (which disrupts the mucosal barrier), where it binds to macromolecules to form a full antigen. This induces an abnormal immune response, leading to the release of pro-inflammatory cytokines and localized chronic inflammation. This model simulates substantial organ damage caused by immune system dysregulation, and its pathological evolution (from acute to chronic) closely mirrors the clinical manifestations of human immune-mediated intestinal injury.

Research Applications

  1. Pathogenesis Research: Exploring the mechanisms of immune system dysregulation and abnormal immune responses in organ injury.
  2. Drug Screening and Evaluation: Evaluating the intervention effects and mechanisms of potential drugs on immune-mediated inflammation.
  3. Chronic Inflammation Evolution Research: Simulating the pathological process of organ damage transitioning from acute to chronic persistent injury.

Key Points of Experimental Design

  • Species: Primarily rodents, commonly rats (SD or Wistar) or mice.
  • Reagents: 2,4,6-Trinitrobenzenesulfonic acid (TNBS) solution and a specific concentration of ethanol.
  • Key Steps:
    1. Mix the TNBS and ethanol solutions in a specific ratio.
    2. Administer via enema so the drug directly affects the colonic mucosa.
    3. Utilize ethanol to disrupt the mucosal barrier, allowing TNBS to form a full antigen and trigger an immune response.

Key Monitoring Indicators

  • Disease Activity Index (DAI) Score: Dynamic evaluation of body weight changes, stool consistency (e.g., loose stools), and occult blood.
  • Histopathological Evaluation:
    • H&E Staining: Assessment of colonic structural destruction under light microscopy.
    • Inflammatory Infiltration Assessment: Observing and scoring the infiltration of inflammatory cells.
  • Gross Morphological Damage Score: Visual observation of colonic tissue adhesions, localized edema, ulcer formation, and the extent of lesions.
  • Immune-related Factor Monitoring: No records available based on current data.