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Review Article

氮氧化应激，高级糖化终产物与炎症性肠病中炎症的密切相互作用

卷 27, 期 13, 2020

页: [2059 - 2076] 页: 18

弟呕挨: 10.2174/0929867325666180904115633

价格: $65

摘要

背景：炎症性肠病（IBD）没有明确的病因。但是，诸如遗传和硝基氧化应激等因素与慢性炎症和IBD进展为结直肠癌（CRC）有关。本综述讨论了IBD中硝基氧化应激，炎症和高级糖基化终产物（AGE）及其相应受体（RAGE）的关联，并探讨了这些因素与核因子之间的联系，例如核因子Kappa B（NF- κB），类红细胞2相关因子2（Nrf2）和p53突变体（p53M）。 方法：我们使用以下术语的组合搜索了PubMed，ScienceDirect和Web of Science数据库：IBD，CRC，氧化应激，炎症，NF-κB，Nrf2，p53M，AGE和RAGE。 结果：氧化应激和炎症激活了两个细胞途径，基于NF-κB和p53M的促炎，促氧化剂和促癌基因的核表达，与NF-κB激活，脱氧核糖核酸（DNA）损伤有关和致癌基因的表达。 Nrf2刺激酶和非酶抗氧化剂系统和抗炎基因的核表达，并被慢性氧化应激，NF-κB和p53M抑制。 AGE / RAGE与炎症进程有关，因为在IBD患者中发现RAGE多态性和RAGE水平升高。这些途径的改变与氧化性损伤的结合是IBD症状和CRC进展的原因。 结论：IBD是一种基于炎症和硝基氧化应激的肠病。对生化事件及其复杂相互作用的分子理解将影响基础和应用研究，动物模型和临床试验。

关键词: 核因子κB，脂多糖，促红细胞因子2-相关因子-2，p53突变体，结直肠癌，脱氧核糖核酸。

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