AI Article Synopsis
- Inflammation caused by H. pylori infection is influenced by the activation of NOD1 through peptidoglycan found in bacterial cell walls, triggering specific inflammatory signaling pathways.
- A new compound, 2-chloroquinazolin-4-ol, has been developed as an effective antagonist to human and mouse NOD1, reducing various inflammatory cytokines and chemokines in immune and epithelial cells.
- The findings suggest that this compound could serve as a potential treatment for gastritis linked to H. pylori infection.
Article Abstract
() infection is characterized by the complex interplay between and gastric disorders. It has been established that NOD1 can be activated by the peptidoglycan (PGN) present in the cell wall of , serving as a key mediator of inflammation and initiating the RIP2/NF-κB and MAPK inflammatory signaling pathways. In this article, we reported on the development of a 2-chloroquinazolin-4-ol derivative as a potent and selective antagonist of both human and mouse NOD1, which effectively inhibited the expression of inflammatory cytokines (IL-6, TNF-α) and chemokines (CXCL1, CXCL8) in immune and epithelial cells, as well as inflammatory cytokines (KC, IL-6) in a -induced murine model of gastritis following oral administration. This study laid a foundation for treating gastritis induced by infection.
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| http://dx.doi.org/10.1021/acs.jmedchem.4c02139 | DOI Listing |
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