Blueberry anthocyanin extracts protect against Helicobacter pylori-induced peptic epithelium injuries both in vitro and in vivo: the key role of MAPK/NF-κB pathway

The protective effects of BE against LPS-induced injuries in mouse stomach depended on the inhibition of both MAPK pathway and the downstream NF-κB signaling.

Peptic injures were induced in a mouse model using LPS plus ligation method and then the mice were treated with BE. Then changes in gastric histology, inflammatory response, and MAPK/NF-κB axis were detected. To reveal the role of MAPK/NF-κB axis in the effects of BE, human gastric epithelial cells (HGECs) were further subjected to co-treatment of BE, LPS, and MAPK activator.

Anthocyanins are well-characterized by anti-oxidative and anti-inflammatory potentials. Peptic ulcers contribute to the development of severe gastric disorders. In the current study, the effects of blueberry anthocyanin extracts (BE) on the Helicobacter pylori lipopolysaccharide (LPS)-induced peptic epithelium injures were assessed and the associated mechanism driving the effects was explored by focusing on MAPK/NF-κB pathway.

The assays of mouse model showed that BE attenuated gastric epithelial injuries by improving epithelial structure and suppressing gastric inflammatory response, which was associated with the inhibition of MAPK/NF-κB axis. In in vitro assays, BE suppressed viability and production of cytokines, and induced apoptosis in LPS-treated HGECs. The re-activation of MAPK pathway counteracted the effects of BE by re-inducing cell viability and suppressing cell apoptosis. Conclusions: The protective effects of BE against LPS-induced injuries in mouse stomach depended on the inhibition of both MAPK pathway and the downstream NF-κB signaling.