Acute Gastric Mucosal Injury Model
Acute Gastric Mucosal Injury Model
We provides highly reproducible preclinical Acute Gastric Mucosal Injury models, including ethanol, NSAID (indomethacin), and stress-induced platforms.
Species & Strain
Sprague-Dawley (SD) / Wistar rats, New Zealand White rabbits, and Bama mini-pigs.
Model Description
Utilizing clinically relevant chemical inductions (ethanol, NSAIDs, or pyloric ligation) and physiological stress, our models accurately replicate acute gastric pathology. These systems feature rapid mucosal exfoliation, hemorrhagic erosion, mucosal barrier compromise, and localized inflammatory storms.
Indication / Application
Preclinical efficacy testing of gastroprotective agents and antisecretory drugs (such as H2 receptor antagonists, PPIs, and P-CABs), screening of mucosal barrier restorers, safety evaluation of ulcerogenic compounds, and mechanistic studies on mucosal microcirculatory perfusion.
Modeling Method
Chemical & Drug-Induced Platforms (Standard Pharmacological Efficacy):
- Ethanol-Induced Model (Gold Standard for Mucosal Defense): Fasted animals receive absolute or 70%–80% ethanol via oral gavage, triggering immediate vascular spasm, mucosal desquamation, and linear hemorrhagic lesions within 1 to 4 hours.
- NSAID-Induced Model (Clinical Pathology Homology): Systemic or oral administration of nonsteroidal anti-inflammatory drugs (e.g., indomethacin, aspirin) to inhibit cytoprotective prostaglandins, inducing multifocal mucosal erosion and punctate ulcers.
Physiological & Surgical Platforms:
- Water Immersion Restraint Stress (WIRS): Animals are restrained and partially immersed in cool water (20°C–22°C) to induce neurogenic, stress-driven mucosal ischemia and acute bleeding.
- Pyloric Ligation (Shay’s Gastric Ulcer): Surgical ligation of the pylorus leads to the accumulation of aggressive gastric acid and pepsin, driving severe self-digestion and gastric ulcers within hours.
Clinical Relevance
- Pathological Homology: The models successfully mirror human acute gastric mucosal lesions triggered by alcohol abuse, stress (such as ICU stress ulcers), or chronic NSAID therapy, displaying classical mucosal hyperemia, edema, and cellular necrosis.
- Precision Drug Evaluation: Utilizing these distinct induction pathways enables sponsors to determine whether a test candidate works via direct mucosal physical barrier reinforcement (ethanol model), prostaglandin-mediated cytoprotection (NSAID model), or acid-secretion blockade (Shay model).
- Translational Scale in Large Animals: For advanced formulations (such as in situ forming hydrogels, barrier-forming sprays, or endoscopic powders), our Bama mini-pig model provides a human-scale clinical platform for endoluminal spraying, retention assessment, and translation evaluation.
Key Evaluation Endpoints
In Vivo & Macroscopic Evaluation
- Gastric Ulcer Index (UI) Assessment: Semi-quantitative macroscopic scoring of the stomach following ex vivo opening along the greater curvature.
- Percentage Inhibition / Curative Ratio: Calculation of the therapeutic compound's relative mucosal protection compared to the untreated control group.
- Gastric Secretion Profiling (Pyloric Ligation): Quantitative measurement of total gastric juice volume, free acidity, and total acid output.
Biochemical & Antioxidant Profiling
- Mucosal Cytoprotective Quantitation: Measurement of gastric wall mucus content (Alcian Blue binding assay) and mucosal Prostaglandin E2 (PGE2) concentrations via ELISA.
- Oxidative Stress Ensembles: Tracking of mucosal Malondialdehyde (MDA) accumulation, alongside Superoxide Dismutase (SOD), Catalase (CAT), and Glutathione (GSH) depletion.
Histopathology & Immunohistochemistry
- Histomorphological Damage Indexing: H&E staining to score the depth of mucosal erosion, glandular disruption, congestion, and infiltration of inflammatory polymorphonuclear leukocytes (PMNs).
- Mucosal Regeneration & Apoptosis Profiling: IHC tracking of Ki-67 (proliferative activity) and PCNA, paired with TUNEL assays to calculate the apoptotic index of the gastric epithelium.
- Localized Inflammatory Cytokines: Quantitation of mucosal and systemic pro-inflammatory markers (such as TNF-alpha, IL-1beta, IL-6, and MPO activity) via RT-qPCR, Western Blot, or ELISA.
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