To study the activity and the underlying mechanism of active alcohols (AA) in Maotai-flavor Baijiu against the damages in gastric mucosal epithelial cells induced by Helicobacter pylori, the minimum half inhibitory concentration (MIC50) of AAs against the H. pylori and the inhibition of H.pylori damage to GES-1 cells by phenethyl alcohol (AA-29) were detected. The influence of AA-29 on H. pylori urease activity was analyzed by ELISA. Furthermore, RT-PCR was used to analyze the transcription of H. pylori urease gene clusters (ureA, ureB, ureE, ureH, ureI and nixA), outer membrane protein genes (babA) and virulence genes (cagA and vacA) after the AA-29 treatments. Western blotting was used to detect the effect of AA-29 on the expression of cagA and vacA. ELISA and flow cytometric detection were used to detect the effect of AA-29 on TNF-α, IL-1β, IL-6 expressions and apoptosis of GES-1 cells induced by H. pylori. Results showed that AA-29 performed the most protective activity and significantly inhibited the growth of H. pylori. The MIC50 (72 h) of AA-29 was 105.2 μg/mL; AA-29 (100 μg/mL) significantly inhibited the urease activity of H. pylori; RT-PCR results showed that AA-29 inhibited the transcription of H. pylori urease gene clusters (ureA, ureB, nixA) and outer membrane protein gene (babA) and virulence gene (cagA). AA-29 also inhibited the expression of cagA. AA-29 inhibited H. pylori-induced TNF-α, IL-1β, IL-6 secretion and GES-1 cell apoptosis. The alcohols in Maotai-flavor Baijiu performed anti-H. pylori activity, and AA-29 inhibited the expression of H. pylori urease related genes and inhibited the H. pylori urease activity. AA-29 attenuated the damages induced by H.pylori in gastric epithelial cells by inhibiting the H.pylori babA, cagA transcription and cagA expression.
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