A study on the antibacterial efficacy and action mechanism of clove against Helicobacter pylori

Background This study aimed to investigate the anti- Helicobacter pylori ( H. pylori ) effects of clove ( Syzygium aromaticum ) and its underlying mechanisms. Method Network pharmacology was used to identify potential targets of clove against H. pylori , followed by GO and KEGG enrichment analyses. Molecular docking was performed to evaluate the binding of key clove-derived compounds to core targets. In vitro antimicrobial susceptibility testing against the H. pylori SS1 strain was conducted to determine antibacterial activity, and an H. pylori infected rat model was used to assess the in vivo anti-inflammatory effects of clove. Result Network pharmacology identified six bioactive components and 19 overlapping targets, among which TP53, MMP9, IL1B, IL10, and TNF were central nodes. Docking analysis showed favorable binding between major compounds and core targets, with quercetin exhibiting the lowest binding energy toward MMP9 (−10.5). In vitro , kaempferol, quercetin, and stigmasterol inhibited H. pylori SS1, with MIC/MBC values of 0.5/1, 2.5/10, and 3.13/12.52 mg/mL, respectively, whereas strictosamide showed weak activity (MIC 10 mg/mL, no detectable MBC) and β-sitosterol did not exhibit quantifiable MIC or MBC values within the tested range. In vivo , clove treatment dose-dependently reduced gastric TNF-α, IL-12, IL-17, IL-23, and IFN-γ levels in H. pylori infected rats and was associated with increased IL-10 expression, particularly in the medium- and high-dose groups at both the protein and mRNA levels. Clove also reduced the elevated protein and mRNA expression levels of IL-1β, MMP9, TP53, and TLR4 in gastric tissue. Conclusion These findings suggest that clove contains constituents with direct in vitro anti- H. pylori activity and may exert anti-inflammatory and gastroprotective effects in H. pylori infected rats. The observed changes in cytokines and inflammation-related molecules support the potential involvement of TNF- and TLR4-associated signaling, although further studies are required to verify direct pathway regulation and in vivo antibacterial mechanisms.