尼古丁胺胺氨基二核酸通过Nrf2/HO-1通路缓解肠道缺血/反损伤
Su-Ying Chen1, Hui Xu2, Yan Qin3
1Department of Radiology, Affiliated Hospital 2 of Nantong University, Medical School of Nantong University, Nantong 226001, China; Nantong Institute of Genetics and Reproductive Medicine, Affiliated Maternity & Child Healthcare Hospital of Nantong University, Nantong 226001, China; Department of Ultrasonography, Wuxi City Rehabilitation Hospital, Liangxi District Chinese Medicine Hospital, Wuxi 214000, China.
International immunopharmacology
|October 29, 2024
概括
降低的尼古丁胺胺氨基二核酸盐 (NADPH) 通过减少炎症和氧化应激来防止肠道缺血-再输液损伤. 它还加强了肠道屏障,并通过Nrf2/HO-1通道平衡了微生物群.
科学领域:
- 胃肠病学 胃肠病学
- 免疫学 免疫学 免疫学
- 生物化学 生物化学
背景情况:
- 肠道缺血-再输液 (I/R) 损伤带来了严重的临床挑战,患病率和死亡率高.
- 在其他器官中降低尼古丁胺胺氨基二核酸盐 (NADPH) 的保护作用表明在肠道I / R损伤中具有潜在的治疗益处.
研究的目的:
- 阐明NADPH对肠道I/R损伤的保护机制.
- 研究Nrf2/HO-1通路在调解NADPH作用中的作用.
主要方法:
- 在体外氧气-葡萄糖剥夺-再氧化和小鼠肠道I / R模型中使用.
- 使用ML385.5进行内NADPH的施用,并抑制Nrf2/HO-1通路.
- 评估了炎症标志物 (IL-1β,NLRP3炎症体),氧化应激标志物,谷氨水平,肠道屏障完整性 (zonula occludens-1) 和肠道微生物组合.
主要成果:
- NADPH的使用降低了IL-1β水平和NLRP3炎症酶激活,减轻了炎症.
- NADPH降低了氧化应激标志物和增加了谷氨水平,显示出抗氧化作用.
- NADPH改善了肠道屏障的完整性,并促进了平衡的肠道微生物组.
- 抑制Nrf2/HO-1通路取消了NADPH的保护作用.
结论:
- 通过抗氧化,抗炎,微生物群平衡和屏障增强机制,NADPH可以保护肠道I / R损伤.
- Nrf2/HO-1信号通路对于调解NADPH在肠道I/R损伤中的治疗益处至关重要.
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