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. <?spacebefore 0.5?>Graphical abstract <?tk 1?>Thirty Wistar albino female rats were divided equally into 5 groups. Group 2–4 rats received indomethacin (5 mg/kg) by gavage for 5 days [<CitationRef CitationID="CR1">1</CitationRef>]. Group 2–4 rats with gastritis were given 1 mL of H. pylori suspension prepared as 10⁸-109 CFU/mL by gavage twice daily for 7 days [<CitationRef CitationID="CR2">2</CitationRef>]. Rats in group 3 received 10 µg/kg melittin by gavage once daily [<CitationRef CitationID="CR3">3</CitationRef>]. Rats in group 4 received 40 µg/kg melittin by gavage once daily [<CitationRef CitationID="CR4">4</CitationRef>]. Group 5 received standard drugs (amoxicillin, 50 mg/kg; clarithromycin, 25 mg/kg; omeprazole, 20 mg/kg) once daily [<CitationRef CitationID="CR5">5</CitationRef>]. After 30 days of treatment, all animals in the groups were euthanized [<CitationRef CitationID="CR6">6</CitationRef>] and gastric tissues were removed [<CitationRef CitationID="CR7">7</CitationRef>]. Gastric tissues were used for microbiological (urease and bacterial count), ELISA (IL-10 and IL-1β), gene expression (HIF-1α and TGF-β), oxidative stress (TOS, TAS, MDA, CAT, GSH) and immunohistochemical (Hematoxylin and eosin and Giemsa) analyses.

Antibacterial and immuno-oxidative effects of Melittin against Helicobacter pylori: in vitro and in vivo evidence

期刊论文
发表日期：

2025年12月5日

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Elif Aydin,
Sema Cetinkaya,
Ayse Kocak Sezgin,
Meliha Koldemir Gunduz,
Birkan Açikgoz,
Sercan Simsek,
Güllü Kaymak

摘要

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.

Graphical abstract

Thirty Wistar albino female rats were divided equally into 5 groups. Group 2–4 rats received indomethacin (5 mg/kg) by gavage for 5 days [1]. Group 2–4 rats with gastritis were given 1 mL of H. pylori suspension prepared as 10⁸-109 CFU/mL by gavage twice daily for 7 days [2]. Rats in group 3 received 10 µg/kg melittin by gavage once daily [3]. Rats in group 4 received 40 µg/kg melittin by gavage once daily [4]. Group 5 received standard drugs (amoxicillin, 50 mg/kg; clarithromycin, 25 mg/kg; omeprazole, 20 mg/kg) once daily [5]. After 30 days of treatment, all animals in the groups were euthanized [6] and gastric tissues were removed [7]. Gastric tissues were used for microbiological (urease and bacterial count), ELISA (IL-10 and IL-1β), gene expression (HIF-1α and TGF-β), oxidative stress (TOS, TAS, MDA, CAT, GSH) and immunohistochemical (Hematoxylin and eosin and Giemsa) analyses.