Research Information System
Molecular Biology Reports, vol.53, no.1, 2026 (SCI-Expanded, Scopus)
Background: Helicobacter pylori (H. pylori) is a common pathogen that causes serious pathologies such as gastritis, ulcers, and gastric cancer. This study evaluates the therapeutic effects of melittin on H. pylori induced gastric injury, oxidative stress, and tissue damage in an in vivo model. Methods and results: Melittin was administered at two doses (10 µg/kg and 40 µg/kg) and outcomes were compared with standard antibiotic therapy. H. pylori infection significantly increased gastric urease activity, the pro-inflammatory cytokine IL-1β, and oxidative stress markers total oxidant status (TOS) and malondialdehyde (MDA); these increases were suppressed by melittin treatment. Melittin also enhanced antioxidant capacity total antioxidant status (TAS) and glutathione (GSH) and supported gastric tissue healing by reducing inflammation and neutrophil activity. Notably, 10 µg/kg melittin led to a ~ 74% reduction in bacterial colony counts and decreased tissue damage. Histopathology confirmed that melittin lowered H. pylori colonization and inflammation scores. Furthermore, the higher dose (40 µg/kg) showed more limited effects on oxidative stress than the lower dose. GSH levels improved with melittin. Conclusions: Melittin demonstrates antibacterial and anti-inflammatory activity against H. pylori associated gastric pathology, with several outcomes favoring the lower dose (10 µg/kg). These findings indicate melittin as a promising therapeutic candidate; however, additional comprehensive studies are needed to support clinical translation.