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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