• Modeling Mechanism：

  L-Arginine hydrochloride, as a substrate of nitric oxide synthase (NOS), can dilate blood vessels in the gastric mucosa, increase blood flow, and at the same time reduce myeloperoxidase (MPO) activity, reduce inflammatory infiltration, and promote ulcer healing.

• Related Products：

  L-Arginine hydrochloride (T0670)

• Modeling Method：

  Experimental Subject：

  Mice, Swiss Albino mice, Male, 6–8 weeks old, 25–30 g

  Dosage and Administration Route：

  Indomethacin 18 mg/kg, Oral (single dose, ulcer induction);Resveratrol 10 mg/kg, Oral (starting 6 hours after ulcer induction, once daily); L-Arginine hydrochloride 25-75 mg/kg, Intraperitoneal injection (administered concurrently with resveratrol, once daily)

  Dosing Frequency and Duration Model：

  Indomethacin single dose, resveratrol and L-arginine hydrochloride administered once daily until ulcer healing (maximum 15 days).

• Validation：

  The ulcer damage score (DS) decreased, with the L-arginine 75 mg/kg group showing significant improvement compared to the resveratrol group; MPO activity decreased, and inflammatory cell infiltration was reduced; NO synthesis in gastric tissue increased, and the eNOS/iNOS ratio increased; PGE₂ synthesis gradually recovered, and ulcer mucosal healing was accelerated.

*Precautions： All mice were sacrificed in batches at 1, 4, 7, and 15 days after modeling, and gastric tissue samples were collected simultaneously. Mice were fasted for 24 hours before indomethacin induction (with free access to water).

*References：Guha P, et,al. Pro-ulcer effects of resveratrol in mice with indomethacin-induced gastric ulcers are reversed by L-arginine. Br J Pharmacol. 2010 Feb 1;159(3):726-34.

• Modeling Mechanism：

  L-Arginine hydrochloride is metabolized to produce large amounts of nitric oxide (NO). NO reacts with oxygen free radicals to produce toxic peroxynitrite, which damages pancreatic acinar cells. At the same time, it interferes with pancreatic enzyme secretion, leading to pancreatic tissue edema, necrosis and inflammatory infiltration, which in turn indirectly damages the intestinal mucosal barrier and causes intestinal flora imbalance.

• Related Products：

  L-Arginine hydrochloride (T0670)

• Modeling Method：

  Experimental Subject：

  Mice, C57BL/6J, Male, 20–22 g, 6–8 weeks old

  Dosage and Administration Route：

  4 g/kg, 10% L-Arginine, dissolved in distilled water and administered intraperitoneally

  Dosing Frequency and Duration Model：

  Administered twice at 1-hour intervals

• Validation：

  Serum lipase activity was significantly increased, calcium ion concentration was significantly decreased, and pancreatic MPO expression was upregulated; small intestinal villus necrosis, edema, and inflammatory cell infiltration were observed, and Occludin and ZO-1 expression was decreased; the richness and diversity of the gut microbiota decreased, with increased abundance of Bacteroidetes and Proteobacteria and decreased abundance of Firmicutes.

*Precautions： Seventy-two hours after modeling, the mice were anesthetized and euthanized by cervical dislocation.

*References：Zhang P,et,al.Comprehensive analysis of intestinal barrier function and microbial diversity changes in L-arginine-induced acute pancreatitis mice. Eur J Med Res. 2025 Sep 29;30(1):912.