Helicobacter pylori (H. pylori) infection is characterized by the complex interplay between H. pylori and gastric disorders. It has been established that NOD1 can be activated by the peptidoglycan (PGN) present in the cell wall of H. pylori, 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 66 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 H. pylori-induced murine model of gastritis following oral administration. This study laid a foundation for treating gastritis induced by H. pylori infection.

中文翻译：

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选择性拮抗 NOD1 介导的炎症信号通路可减轻幽门螺杆菌感染诱导的胃炎


幽门螺杆菌 （H. pylori） 感染的特征是幽门螺杆菌与胃部疾病之间复杂的相互作用。已经确定 NOD1 可被幽门螺杆菌细胞壁中存在的肽聚糖 （PGN） 激活，作为炎症的关键介质并启动 RIP2/NF-κB 和 MAPK 炎症信号通路。在本文中，我们报道了 2-氯喹唑啉-4-醇衍生物 66 作为人和小鼠 NOD1 的有效和选择性拮抗剂的开发，它有效抑制免疫细胞和上皮细胞中炎性细胞因子 （IL-6、TNF-α） 和趋化因子 （CXCL1、CXCL8） 的表达，以及幽门螺杆菌中炎性细胞因子 （KC、IL-6） 的表达- 口服给药后诱导的小鼠胃炎模型。本研究为治疗幽门螺杆菌感染引起的胃炎奠定了基础。