Zvast Biotechnology
Indomethacin-induced
The indomethacin-induced gastric ulcer model in rats is a SCI gold-standard standardized animal model for simulating clinical drug-induced acute gastric ulcer based on non-steroidal anti-inflammatory drug (NSAID) toxic injury. It focuses on the core pathological mechanism of cyclooxygenase inhibition-oxidative stress imbalance-inflammatory cascade activation-gastric mucosal barrier damage, and highly recapitulates acute gastric mucosal congestion, edema, erosion and ulcerative lesions caused by long-term or excessive clinical NSAID administration. As a typical non-selective cyclooxygenase (COX) inhibitor, indomethacin potently inhibits the activities of COX-1 and COX-2, significantly blocks the synthesis of prostaglandins (PGE2, PGI2) in gastric mucosa, destroys the inherent protective system of gastric mucosa, reduces mucosal blood flow, inhibits mucus and bicarbonate secretion, and impairs the anti-injury ability of gastric mucosa. Meanwhile, indomethacin induces massive ROS accumulation and antioxidant system depletion in gastric tissues, activates the classic NF-κB inflammatory pathway, and promotes the massive release of pro-inflammatory factors such as TNF-α, IL-6 and IL-1β, causing severe local inflammatory infiltration, vascular endothelial injury and microcirculation disturbance in gastric mucosa, and finally stably forming typical acute gastric ulcer phenotypes including punctate erosion, cord-like ulceration, congestive hemorrhage and mucosal exfoliation. SD rats have stable gastric tissue structure, sensitive response to indomethacin drug toxicity, high modeling phenotype uniformity, minimal individual differences and no spontaneous self-healing, which serves as the international gold-standard model for research on drug-induced gastric ulcer pathogenesis, gastric mucosal barrier protection, anti-ulcer new drug screening and NSAID gastrointestinal toxicity protection, and is widely applicable for basic mechanism research and preclinical pharmacodynamic evaluation.
The gastric mucosa of rats in the blank control group was intact and smooth with ruddy color, no congestion, edema, erosion or damage. The model group presented typical acute gastric mucosal injury phenotypes: extensive mucosal congestion and edema, punctate or cord-like erosion, superficial ulceration and local hemorrhagic ecchymosis with clear and uniformly distributed ulcer boundaries. The ulcer index of the model group was significantly higher than that of the blank control group with statistically significant inter-group differences, and the macroscopic phenotype conforms to the characteristics of indomethacin-induced drug gastric ulcer, confirming successful modeling.
HE staining of gastric tissues showed typical pathological changes of drug-induced gastric ulcer: exfoliation of gastric mucosal epithelial cells, destruction of mucosal integrity, disordered and atrophic gastric glands, diffuse infiltration of a large number of inflammatory cells in the lamina propria, interstitial congestion, edema, vasodilation and hemorrhage, and local mucosal defects without deep muscular layer necrosis, which accurately corresponds to the pathological characteristics of clinical NSAID-induced acute superficial gastric ulcer with stable and typical modeling phenotypes.
The contents of oxidative damage products ROS and MDA in gastric tissues of the model group were significantly increased, while the activities of antioxidant enzymes SOD and GSH-Px were significantly decreased, resulting in severe oxidative stress imbalance and intense lipid peroxidation damage in gastric mucosa, which conforms to the core mechanism of indomethacin-induced gastric mucosal oxidative damage and serves as one of the key quantitative criteria for successful modeling.
The expression of core pro-inflammatory factors (TNF-α, IL-6, IL-1β) in gastric tissues of the model group was significantly upregulated with excessive activation of inflammatory pathways. Meanwhile, the content of gastric mucosal protective factor PGE2 was significantly decreased, the expression of tight junction proteins was reduced, and the gastric mucosal barrier function was severely damaged, which fully conforms to the core pathological mechanism of indomethacin inhibiting cyclooxygenase, destroying mucosal protection and inducing inflammatory ulceration, serving as the core academic gold standard for successful model construction.
As an exclusive SCI gold-standard model for NSAID-induced drug gastric ulcer, it accurately recapitulates the real pathological process of clinical drug-induced acute gastric mucosal injury with a single and clear mechanism and high specificity, without interference from Helicobacter pylori, ethanol and other interventions. It features a short modeling cycle, simple operation, one-dose successful modeling, low experimental cost and excellent reproducibility. The gastric mucosal injury phenotype of rats is stable with minimal intra-group differences, zero animal mortality and high safety. It perfectly focuses on the classic mechanisms of cyclooxygenase inhibition, prostaglandin deficiency, oxidative inflammatory injury and mucosal barrier destruction, with clear project mechanism innovation and highly recognized data. It is suitable for pharmacodynamic evaluation and mechanism research of anti-ulcer traditional Chinese medicine, natural active ingredients, gastric mucosal protective preparations and anti-inflammatory and antioxidant drugs, fully meeting the requirements for project declaration, master and doctoral theses and high-score SCI publication.
The indomethacin-induced gastric ulcer model in rats is corely applied to the research of NSAID gastrointestinal toxicity mechanism, gastric mucosal oxidative inflammatory injury and mucosal barrier regulation mechanism. It is specially used to evaluate the core pharmacodynamic effects of various drugs on protecting gastric mucosa, anti-ulcer, anti-oxidation, anti-inflammation and repairing mucosal barrier. It is widely suitable for the intervention and protection research of traditional Chinese medicine compounds, natural active ingredients, small chemical molecules and functional preparations on drug-induced gastric injury, serving as an essential core standardized model in the fields of digestive pharmacology, gastrointestinal mucosal protection and anti-inflammatory drug development, and adapting to various basic and translational medical projects related to gastric ulcer.
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