Galangin Alleviates Helicobacter pylori Gastritis Through TLR2 Inhibition and Modulation of the MyD88 ‐Dependent Inflammatory Cascades

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BACKGROUND: Excessive inflammatory response represents the primary pathological hallmark of Helicobacter pylori (H. pylori) gastritis. Toll-like receptor 2 (TLR2) has emerged as a promising therapeutic target because of its crucial role in regulating inflammatory responses and tissue damage caused by H. pylori. Galangin (Gal), a naturally occurring flavone, possesses a variety of pharmacological activities, including anti-inflammatory and antibacterial effects. This study systematically evaluates the therapeutic potential of Gal in H. pylori gastritis, with specific emphasis on elucidating its TLR2-targeting mechanism. MATERIALS AND METHODS: An H. pylori-induced mouse gastritis model was established to evaluate the therapeutic effects of Gal at dosages of 50 and 100 mg/kg/day over a two-week administration period. The H. pylori-infected GES-1 human gastric epithelial cells were utilized for mechanistic exploration. Molecular docking and siRNA transient transfection techniques were integrated to elucidate the specific interactions between Gal and TLR2. RESULTS: Gal inhibited the proliferation of H. pylori and alleviated the inflammation caused by H. pylori in both in vitro and in vivo. Furthermore, Gal inhibited the activation of the TLR2/MyD88 signaling pathway, which suppressed the downstream phosphorylation of MAPK (p38/JNK/ERK) and NF-κB nuclear translocation. Notably, the knockdown of TLR2 diminished the inhibitory effects of Gal on MyD88 expression. CONCLUSION: Gal demonstrated effectiveness in ameliorating H. pylori gastritis through the therapeutic inhibition of TLR2. Further investigation is warranted to explore the combination of Gal with other H. pylori eradication treatments.

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