PURPOSE: 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. METHODS: 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. RESULTS: 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.
PURPOSE: 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. METHODS: 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. RESULTS: 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.
Authors: Carlo A Fallone; Naoki Chiba; Sander Veldhuyzen van Zanten; Lori Fischbach; Javier P Gisbert; Richard H Hunt; Nicola L Jones; Craig Render; Grigorios I Leontiadis; Paul Moayyedi; John K Marshall Journal: Gastroenterology Date: 2016-04-19 Impact factor: 22.682
Authors: P Malfertheiner; F Megraud; C A O'Morain; J P Gisbert; E J Kuipers; A T Axon; F Bazzoli; A Gasbarrini; J Atherton; D Y Graham; R Hunt; P Moayyedi; T Rokkas; M Rugge; M Selgrad; S Suerbaum; K Sugano; E M El-Omar Journal: Gut Date: 2016-10-05 Impact factor: 23.059
Authors: H Zojaji; R Talaie; D Mirsattari; M Haghazali; M Molaei; N Mohsenian; F Derakhshan; M R Zali Journal: Dig Liver Dis Date: 2009-06-02 Impact factor: 4.088