Galangin Alleviates Helicobacter pylori Gastritis Through TLR2 Inhibition and Modulation of the MyD88-Dependent...

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.

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.

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.

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.