Gastric Ulcer Model
Gastric Ulcer Model
HuaTeng Biotechnology offers a high-fidelity preclinical platform for both acute gastric ulcers and chronic, healing-delayed gastric ulcers.
Species & Strain
Sprague-Dawley (SD) / Wistar rats, C57BL/6 mice, and Bama mini-pigs.
Model Description
Unlike superficial mucosal injuries, our ulcer models penetrate deep into the muscularis mucosae. Our capabilities feature the benchmark acetic acid-induced chronic ulcer model (Okabe’s method) along with clinically relevant NSAID and pyloric ligation systems. This platform is specifically designed to study the dynamic, cellular processes of gastric tissue remodeling, angiogenesis, and mucosal scar formation, supporting the evaluation of novel ulcer-healing therapeutics, proton pump inhibitors (PPIs), mucosal protectants, and bio-scaffolds under strict OECD GLP and AAALAC compliance.
Indication / Application
Efficacy validation of ulcer-healing therapeutics, assessment of long-acting gastric mucosal repair agents, screening of antisecretory agents (H2RAs, PPIs, P-CABs), safety and toxicity profiling of ulcerogenic compounds, and mechanistic investigations into growth factor-mediated tissue regeneration.
Modeling Method
Acetic Acid-Induced Chronic Gastric Ulcer Model (Benchmark Assay for Ulcer Healing)
A laparotomy is performed under general anesthesia. A small cylindrical mold is affixed to the serosal surface of the gastric corpus. A precise concentration of glacial acetic acid is briefly applied to the serosal tissue to generate a highly localized, standardized ulcer that penetrates the muscularis mucosae. These lesions closely recapitulate human chronic gastric ulcers and undergo spontaneous healing over 10–14 days, offering an optimal time window to evaluate drug-accelerated ulcer repair.
NSAID & Chemical-Induced Gastric Ulcer Models
High-dose indomethacin, aspirin or absolute ethanol is administered to fasted animals to induce severe hemorrhagic ulcers characterized by distinct necrotic cores and raised mucosal margins.
Pyloric Ligation (Shay Ulcer) Model
Surgical ligation of the pyloric sphincter traps hyperacidic gastric secretions, triggering autodigestion and the formation of multifocal gastric ulcers within the forestomach.
Clinical Relevance
Depth & Chronicity Fidelity
Whereas acute erosion models merely injure the superficial epithelium, our acetic acid-induced model generates bona fide deep ulcer craters with a sloughing necrotic base, recapitulating the pathology of human peptic ulcer disease (PUD).
Dynamic Remodeling Windows
This platform enables sponsors to assess not only mucosal protection but genuine tissue regeneration, permitting evaluation of therapeutic effects on epithelial cell migration, extracellular matrix deposition, and structural restoration of gastric glands.
Human-Scale Translation
Our Bama mini-pig ulcer platform provides clinical-scale anatomical access, enabling endoscopic administration of novel bioadhesives, protective hydrogels, or localized physical barriers.
Key Evaluation Endpoints
In Vivo & Macroscopic Evaluation
- Quantitative Ulcer Index (UI) & Healing Rate (Primary Efficacy Endpoint): Measurement of the physical ulcer area (length × width, mm) and calculation of the percentage of ulcer contraction and healing relative to control groups.
- Gastric Secretion Analysis (Pyloric Ligation): Collection and detection of gastric juice volume, pH value, free acidity, and total acid output.
- Non-Invasive Gastric Endoscopy: Longitudinal, real-time endoluminal imaging to monitor ulcer crater size, margin retraction, and mucosal color recovery.
Histopathology & Mucosal Regeneration (Microstructural Analysis)
- Histomorphometric Assessment: Standard H&E staining for semi-quantitative scoring of mucosal regenerative thickness, granulation tissue depth, inflammatory cell infiltration, and mucosal scar quality.
- Masson's Trichrome & Sirius Red Staining: Visualization and quantification of collagen deposition and extracellular matrix remodeling at the base of healed ulcers.
Angiogenesis & Re-epithelialization Profiling
- Neovascularization: IHC detection of CD31 and VEGF for quantification of microvessel density (MVD) in granulation tissue.
- Cell Proliferation: IHC profiling of Ki-67, PCNA, and EGF/EGFR expression to assess active epithelial regeneration.
Biochemical, Inflammatory & Cytoprotective Profiling
- Mucosal Cytoprotective Markers: Quantitative detection of gastric mucosal prostaglandin E₂ (PGE₂) levels and hexosamine/adherent mucus content.
- Inflammatory Cascade Quantification: Measurement of localized and systemic levels of key pro-inflammatory cytokines (TNF-α, IL-1β, IL-6) and myeloperoxidase (MPO) activity.
- Oxidative Stress Monitoring: Biochemical assays detecting mucosal tissue levels of malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione (GSH).
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