Molecular Mechanisms of Natural Honey Against H. pylori Infection Via Suppression of NF-κB and AP-1 Activation in Gastric Epithelial Cells

Arch Med Res. 2016 Jul;47(5):340-348. doi: 10.1016/j.arcmed.2016.09.002.


Background and aims: Natural honey has been used as a medicine since ancient times. Honey is widely known for its antibacterial properties against H. pylori; however, the mechanisms of its antibacterial activity are not fully known. The present study was performed to examine the molecular mechanisms by which natural honey can inhibit H. pylori infection in gastric epithelial cells.

Methods: Electrophoretic mobility shift assay was used to measure NF-κB- and AP-1-DNA binding activity. Western blotting was used to detect IκB-α and COX-2 expression.

Results: H. pylori induced NF-κB and AP-1 DNA-binding activity in gastric epithelial cells. Manuka honey inhibited H. pylori-induced NF-κB and AP-1 in a time- and dose-dependent manner. Maximum inhibition of H. pylori-induced NF-κB and AP-1 by manuka honey was observed at concentrations of 20% at 1-2 h. Pre-treatment of AGS cells with other commercial natural honeys also inhibited H. pylori-induced NF-κB and AP-1 DNA-binding activity. Honey prevented H. pylori-induced degradation of IκB-α protein and downregulated COX-2 protein levels.

Conclusions: Our findings suggest that natural honey exerts its inhibitory effects against H. pylori by inhibiting NF-κB and AP-1 activation and downregulation of COX-2 expression. These results provide new mechanistic insights into honey effects in the suppression of H. pylori infection.

Keywords: AP-1; Gastric epithelial cells; H. pylori; NF-κB; Natural honey.

MeSH terms

  • Cell Line
  • Cell Survival
  • Cyclooxygenase 2 / metabolism
  • DNA / metabolism
  • Down-Regulation
  • Epithelial Cells / cytology
  • Epithelial Cells / metabolism*
  • Gastric Mucosa / cytology
  • Gastric Mucosa / metabolism
  • Gastric Mucosa / microbiology*
  • Helicobacter pylori / physiology*
  • Honey*
  • Humans
  • NF-kappa B / metabolism*
  • Protein Binding
  • Transcription Factor AP-1 / metabolism*


  • NF-kappa B
  • Transcription Factor AP-1
  • DNA
  • Cyclooxygenase 2