Akademik Veri Yönetim Sistemi
Naunyn-Schmiedeberg's Archives of Pharmacology, 2026 (SCI-Expanded, Scopus)
In this study, the potential protective effects of syringic acid (SA) on gastric tissue were investigated in an indomethacin (INDO)-induced gastric ulcer model. A total of 84 male Sprague–Dawley rats were randomly divided into seven groups. In the in vivo experiments, rats were administered SA at doses of 5, 50, and 100 mg/kg and omeprazole (OMP) at a dose of 5 mg/kg intragastrically (i.g.) for 14 days, and indomethacin (100 mg/kg, i.g.) was administered on the final day. Following INDO administration, the rats were sacrificed under anesthesia, and gastric tissues were carefully excised for further analyses. The collected gastric tissues were subjected to biochemical, histopathological, and immunofluorescence analyses. In addition, in silico analyses were performed to support the INDO-induced gastric ulcer model. Using the licensed Schrödinger Maestro 2025/1 software, the binding properties of INDO to the COX-1 receptor were evaluated through molecular docking, MM-GBSA, and pharmacophore matching analyses. INDO administration was associated with oxidative stress, inflammation, apoptosis, and histopathological damage in gastric tissue. SA treatment appeared to alleviate INDO-induced gastric injury through its antioxidant, anti-inflammatory, and anti-apoptotic properties. SA treatment ameliorated histopathological alterations in ulcerated areas, particularly at doses of 50 and 100 mg/kg, whereas the 5 mg/kg dose did not show a significant protective effect. In addition, in silico analyses suggested that INDO may contribute to ulcer formation by inhibiting COX-1, thereby reducing prostaglandin production in the gastric mucosa. Overall, the findings of this study suggest that SA may reduce oxidative stress, suppress inflammatory responses, and inhibit apoptosis, thereby contributing to the protection of gastric tissue against INDO-induced injury. These results indicate that SA may have therapeutic potential for the prevention of NSAID-induced gastric injury; however, further experimental and clinical studies are needed to confirm these effects and clarify the underlying mechanisms.