• Modeling Mechanism：

  Indomethacin inhibits cyclooxygenase (COX) activity, reduces prostaglandin (PGE) synthesis, and disrupts the small intestinal mucosal repair function. Simultaneously, it damages tight junction proteins, increases intestinal permeability, and triggers local inflammation mediated by gut microbiota and intestinal contents, inducing the release of pro-inflammatory factors such as TNF-α and IL-6. Furthermore, it induces oxidative stress, reduces glutathione (GSH) and antioxidant enzyme (SOD, GPX) activity, and increases lipid peroxidation products (MDA) and total oxygen saturation (TOS), ultimately leading to small intestinal villus structure destruction, erosion, ulceration, and inflammatory infiltration.

• Related Products：

  Indomethacin sodium hydrate (T22346)

• Modeling Method：

  Experimental Subject：

  Rats, Wistar, Female, 15 weeks old, Weight 160-200g

  Dosage and Administration Route：

  25 mg/kg indomethacin, Dissolved in 0.9% saline solution, Administered via gavage

  Dosing Frequency and Duration Model：

  Single dose

• Validation：

  The small intestinal tissue showed disordered villus structure, erosion and ulceration, and inflammatory cell infiltration, with a significantly elevated total pathological damage score; the levels of TNF-α and IL-6 in the small intestinal tissue were significantly elevated; the content of GSH and the activities of SOD and GPX were decreased, while the levels of MDA and TOS were increased; and the total antioxidant level (TAS) of the tissue was decreased.

*Precautions： All rats were anesthetized and sacrificed 6 hours after modeling, and the small intestine tissue was rapidly separated.

*References：Secgin S, et,al. Thiamine pyrophosphate may protect indomethacin-induced small intestinal enteropathy in rats by inhibiting intestinal inflammation and oxidative stress. Naunyn Schmiedebergs Arch Pharmacol. 2025 Oct;398(10):14441-14450.

• Modeling Mechanism：

  Indomethacin sodium hydrate inhibits the synthesis of COX-1/COX-2 prostaglandins, leading to decreased gastric mucosal defense, increased inflammation and oxidative stress, and thus causing gastric mucosal damage and ulcer formation.

• Related Products：

  Indomethacin sodium hydrate (T22346)

• Modeling Method：

  Experimental Subject：

  Rats, Wistar, Equal numbers of males and females, 200-220 g

  Dosage and Administration Route：

  Indomethacin 30 mg/kg, Dissolved in distilled water and administered by gavage

  Dosing Frequency and Duration Model：

  Single dose

• Validation：

  Serum EGF and PGE2 concentrations were significantly decreased. Immunohistochemical results showed that the expression levels of COX-1 and COX-2 in the gastric mucosa were significantly downregulated, and there was significant gastric mucosal epithelial shedding, edema, and inflammatory cell infiltration. The gastric mucosal injury index was significantly increased.

*Precautions： Before administration to all animals 24 hFasting was implemented. In the prevention experiment, animals were sacrificed 6 hours after gavage administration of indomethacin; in the treatment experiment, animals were administered the drug for 3 days after modeling, followed by a 24-hour fast before being sacrificed.

*References：Fang YF,et,al.Effect of Hydrotalcite on Indometacin-Induced Gastric Injury in Rats. Biomed Res Int. 2019 Apr 11;2019:4605748.