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<p>Gastric ulcers result from an imbalance between aggressive factors and protective mechanisms within the gastric mucosa. Simvastatin (SIM), widely prescribed for lipid regulation, has been reported to enhance gastric defense through modulation of prostaglandin E₂ (PGE₂), while gallic acid (GA) is a well-known phenolic antioxidant. This study evaluated the individual and combined gastroprotective effects of SIM and GA against indomethacin (IND) induced gastric ulcers in male Wistar albino rats and explored their interaction with the EP3 receptor using molecular docking (PDB IDs: 6AK3 and 6M9T). Animals were divided into eight groups and pretreated with SIM, GA, or SIM–GA combinations (1:1, 1:2, and 2:1) for 14 days prior to ulcer induction. Gastric protection was assessed by ulcer index, gastric pH, mucus content, glandular stomach weight, total protein levels, myeloperoxidase (MPO) activity, non-protein sulfhydryl (NP-SH) groups, nitric oxide (NO), and histopathological examination. The SIM–GA 1:2 combination produced the most pronounced gastroprotective effect, evidenced by a significant reduction in ulcer index, increased gastric pH and mucus secretion, and preservation of mucosal architecture. Biochemical analyses revealed decreased MPO activity and elevated NP-SH, NO, and protein levels, indicating enhanced antioxidant and cytoprotective responses. Molecular docking study supported these findings, showing stronger binding affinity of SIM and GA toward the EP3 receptor compared with the co-crystallized ligands misoprostol and PGE₂. Overall, the combined administration of SIM and GA, particularly at a 1:2 ratio, demonstrates enhanced gastroprotective potential against NSAID-induced gastric ulceration.</p> Graphical Abstract <p></p>

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Synergistic Gastroprotective Effects of Simvastatin and Gallic Acid in Indomethacin-Induced Gastric Ulcers in Rats

  • 期刊论文

  • 发表日期：

    2026年3月2日

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  • Tanmay Sarma,
  • Trishna Das,
  • Rajana James,
  • Shameem Ara Begum,
  • Ayesha Aktar Khanam Choudhury,
  • Dipankar Saha,
  • Smriti Rekha Chanda Das,
  • Mrinmoy Basak,
  • Sailee Chowdhury,
  • Koyel Kar,
  • Priyanka Chakraborty

摘要

Gastric ulcers result from an imbalance between aggressive factors and protective mechanisms within the gastric mucosa. Simvastatin (SIM), widely prescribed for lipid regulation, has been reported to enhance gastric defense through modulation of prostaglandin E₂ (PGE₂), while gallic acid (GA) is a well-known phenolic antioxidant. This study evaluated the individual and combined gastroprotective effects of SIM and GA against indomethacin (IND) induced gastric ulcers in male Wistar albino rats and explored their interaction with the EP3 receptor using molecular docking (PDB IDs: 6AK3 and 6M9T). Animals were divided into eight groups and pretreated with SIM, GA, or SIM–GA combinations (1:1, 1:2, and 2:1) for 14 days prior to ulcer induction. Gastric protection was assessed by ulcer index, gastric pH, mucus content, glandular stomach weight, total protein levels, myeloperoxidase (MPO) activity, non-protein sulfhydryl (NP-SH) groups, nitric oxide (NO), and histopathological examination. The SIM–GA 1:2 combination produced the most pronounced gastroprotective effect, evidenced by a significant reduction in ulcer index, increased gastric pH and mucus secretion, and preservation of mucosal architecture. Biochemical analyses revealed decreased MPO activity and elevated NP-SH, NO, and protein levels, indicating enhanced antioxidant and cytoprotective responses. Molecular docking study supported these findings, showing stronger binding affinity of SIM and GA toward the EP3 receptor compared with the co-crystallized ligands misoprostol and PGE₂. Overall, the combined administration of SIM and GA, particularly at a 1:2 ratio, demonstrates enhanced gastroprotective potential against NSAID-induced gastric ulceration.

Graphical Abstract