Eudesmin attenuates Helicobacter pylori-induced epithelial autophagy and apoptosis and leads to eradication of H. pylori infection.

Abstract

Eudesmin has been proven to possess anti-inflammatory effects. In the present study, the effects of eudesmin on Helicobacter pylori (H. pylori)-mediated autophagy, apoptosis, immune response and inflammation were determined in human gastric adenocarcinoma (AGS) cells in vitro and in C57BL/6 mice in vivo. Detection of the production of interleukin (IL)-8, IL-1β and immunoglobulin M (IgM) was performed using ELISA. Identification of the activation of apoptosis-associated caspase-3, −8 and −9 proteins, Bcl-2-associated X protein (Bax) and BH3 interacting domain death agonist (Bid) protein, was determined through western blot analysis. Autophagy microtubule-associated protein 1A/1B-light chain 3, isoform B (LC-3B) expression was measured using immunostaining. The results of the present study demonstrated that eudesmin inhibited the growth of H. pylori, with increased inhibition activity against antibiotic resistant strains compared with the reference strain. In addition, H. pylori-induced IL-8 secretion, LC-3B expression and apoptosis-associated protein (caspase-3, −8 and −9, Bax and Bid) activation in AGS cells was suppressed by eudesmin. Furthermore, eudesmin suppressed IL-1β and IgM production in H. pylori-infected C57BL/6 mice in vivo. In conclusion, eudesmin may be developed as a promising therapeutic agent to prevent and/or treat H. pylori-associated gastric inflammation.