Project description:Helicobacter pylori infection reprograms host gene expression and influences various cellular processes, which have been investigated by cDNA microarray in vitro culture cells and in vivo patients of the chronic abdominal complaint. In this study，the effects of H. pylori infection on host gene expression in the gastric antral mucosa of patients with chronic gastritis were examined. The gastric antral mucosa was obtained from a total of 6 untreated patients undergoing gastroscopic and pathologic confirmation of chronic superficial gastritis. Three patients infected by H. pylori and 3 patients uninfected were used to cDNA microarray experiment.
Project description:Ethnopharmacological relevance: Helicobacter pylori (H.pylori) infection is the leading cause of gastric mucosal damage and inflammation, and persistent infection is one of the major risk factors for gastric cancer. Eradication of H.pylori remains a clinical challenge, and therefore, it is urgently necessary to identify more drugs that can interfere with H.pylori colonization and promote its clearance. Jiawei Lianpu Yin (JWLPY) is a compound formula composed of natural drugs used to treat gastric diseases associated with H.pylori infection. However, the underlying mechanisms of its action are still unclear. Aim of the study: The aim of this study was to investigate whether JWLPY can inhibits H.pylori colonization and alleviates gastric mucosal inflammation and damage and to explore its mechanism of action. Materials and METHODS: The effects of JWLPY on Helicobacter pylori and gastric mucosa injury were studied by using Helicobacter pylori induced gastritis model in rats. Transcriptomics, network pharmacology and bioinformatics were used to determine the mechanism of JWLPY Results: JWLPY inhibited the aggregation of inflammatory cells and preserved the integrity of the mucosal barrier, reducing autophagy and apoptosis in gastric mucosal epithelial cells. Network pharmacology and transcriptomics analysis revealed that JWLPY promotes the assembly and synthesis of MUC5AC in the endoplasmic reticulum by activating the IRE1-XBP1 signaling pathway, which enhances the process of protein assembly in the endoplasmic reticulum, thereby inhibiting H.pylori colonization in the gastric mucosa. Conclusion: This study is the first to demonstrate that JWLPY inhibits H.pylori colonization in the gastric mucosa, alleviates gastric inflammation and damage, and is a potential drug for the treatment of H.pylori -related gastritis.
Project description:Even after endoscopic treatment of early gastric adenocarcinoma (GAC) and eradication of Helicobacter pylori (H. pylori), some patients develop a metachronous recurrence (MR), the mechanism of which is still unknown. To elucidate the mechanism and risk factors for MR, we analyzed gene expression at multiple locations of the gastric mucosa, considering the heterogeneity of gastric mucosal damage caused by H. pylori infection and investigated the mechanism and risk factors for MR.
Project description:Helicobacter pylori infection reprograms host gene expression and influences various cellular processes, which have been investigated by cDNA microarray in vitro culture cells and in vivo patients of the chronic abdominal complaint. In this study，the effects of H. pylori infection on host gene expression in the gastric antral mucosa of patients with chronic gastritis were examined.
Project description:Helicobacter pylori (H. pylori) is a human pathogen that infects almost half of the world’s population. Infection with H. pylori is frequently associated with chronic gastritis and can even lead to gastric and duodenal ulcers and gastric cancer. Although the persistent colonization of H. pylori and the development of H. pylori-associated gastritis remain poorly understood, it is believed that, in gastric mucosa, the modulated gastric epithelial cells (GECs) by H. pylori are key contributors. We used microarrays to detail the global programme of gene expression in Helicobacter pylori infected-gastric epithelial cell line AGS cells and identified up-regulated genes induced by Helicobacter pylori infection.
Project description:The whole-genome oligonucleotide microarray analysis gives an opportunity for studying the unidentified gene expression background of the idiopathic and H.pylori related gastric erosive alterations. Using microarrays we compared the whole genome gene expression profile of HP+ and HP- gastric erosions and normal adjacent mucosa to explain the possible role and response to HP infection and to get morphology related mRNA expression patterns. Keywords: whole genomic expression
Project description:Even after endoscopic treatment of early gastric adenocarcinoma (GAC) and eradication of Helicobacter pylori (H. pylori), some patients develop a metachronous recurrence (MR), the mechanism of which is still unknown. To elucidate the mechanism and risk factors for MR, we analyzed gene expression at multiple locations of the gastric mucosa, considering the heterogeneity of gastric mucosal damage caused by H. pylori infection and investigated the mechanism and risk factors for MR.
Project description:The aim of this study is to identify alterations induced in gastric mucosa of mice exposed to Pteridium aquilinum and/or infected with Helicobacter pylori, in order to identify genes that are induced by bracken fern exerts exacerbating effects on gastric lesions associated to the infection.
