Integrated network pharmacology, metabolomics, and transcriptomics of Lianpuyin Jiawei decoction in Helicobacter pylori induced chronic gastritis.

Abstract

ETHNOPHARMACOLOGICAL RELEVANCE: Helicobacter pylori (H. pylori) infection represents the most significant pathogenetic factor for chronic gastritis (CG) and is also the most critical controllable risk factor for the prevention of gastric cancer. Lianpuyin Jiawei Decoction (LPYJWD), a traditional formula originating from Traditional Chinese medicine, has been used to treat H. pylori-induced gastric disorders. Studies have shown that LPYJWD effectively reduce H. pylori-induced gastric mucosal inflammation and improve gastric mucosal damage. However, the potential pharmacological mechanism of LPYJWD requires further elucidation. AIM OF THE STUDY: The present study explored the potential mechanism of LPYJWD in treating H. pylori-induced CG. MATERIALS AND METHODS: The components of LPYJWD entering the bloodstream were identified using UPLC-MS/MS. The H. pylori-induced CG model mice were established by NaHCOand suspension of H. pylori bacteria. Network pharmacology, transcriptome, and metabolomic analyses were integrated to systematically clarify the underlying mechanism of action of LPYJWD against H. pylori-induced CG. Real-time quantitative PCR and Western blot were performed to validate the key mechanisms. RESULTS: LPYJWD was found that 38 potential drug components may exert therapeutic effects. LPYJWD alleviate gastric mucosal inflammation and improve gastric tissue damage of H. pylori-induced CG mice. Metabolomic analysis indicated that LPYJWD affects metabolic pathways, including glycolysis, pentose phosphate, arginine, arachidonic acid, and glycerophospholipid metabolism in gastric mucosal epithelial cells. Network Pharmacology and transcriptome analysis indicated that the LPYJWD may exert therapeutic effects through signaling pathways involving IL-17, TNF, NLRP3, and NF-κB. Further experimental results validated that LPYJWD improves gastric mucosal inflammation through inhibiting the IL-17/NF-κB/NLRP3/signaling pathway. CONCLUSION: Our findings demonstrated that the potential therapeutic benefits of LPYJWD in ameliorating H. pylori-induced CG by targeting the IL-17 signaling pathway, thereby facilitating a more extensive use of LPYJWD in H. pylori-induced CG.