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Nrf2(Nuclear factor-erythroid 2-rdated factor-2)在细胞受到氧化物或亲电子攻击时会及时诱导抗氧化,Ⅱ相解毒酶和相关应激反应蛋白的产生,起到重要的细胞保护作用,是一个关键又重要的转录因子。近来研究表明Nrf2/ARE信号通路也参与抑制炎症相关疾病,如自身免疫疾病、风湿类关节炎、哮喘、肺气肿、胃炎、结肠炎和动脉粥样硬化等。扰乱Nrf2信号不仅会增加机体对氧化物,电子攻击的敏感性,还会加重炎症组织的损伤。在炎症介导的组织损伤早期,Nrf2/ARE的激活可能会抑制促炎介质的产生及表达,包括细胞因子,炎症趋化因子,细胞粘附因子,基质金属蛋白酶,环氧化酶2(COX-2),诱导性一氧化氮合酶(iNOS)。与此同时,Nrf2介导的具有细胞保护能力的下游基因会参与调节先天免疫应答,同时抑制促炎基因的表达。该综述强调Nrf2在炎症相关疾病中的保护作用,侧重此转录因子对炎症信号的调节。
Nrf2 (nuclear factor-erythroid 2-rdated factor-2) in the cells by oxide or electrophilic attack will promptly induce anti-oxidation, phase Ⅱ detoxification enzymes and related stress response protein production, play an important cytoprotective effect, Is a key and important transcription factor. Recent studies have shown that Nrf2 / ARE signaling pathway is also involved in the suppression of inflammation-related diseases such as autoimmune diseases, rheumatoid arthritis, asthma, emphysema, gastritis, colitis and atherosclerosis. Disrupting the Nrf2 signal not only increases the body’s sensitivity to oxide and electron attacks but also aggravates inflammation tissue damage. In the early stage of inflammation-induced tissue damage, Nrf2 / ARE activation may inhibit the production and expression of proinflammatory mediators, including cytokines, inflammatory chemokines, cell adhesion molecules, matrix metalloproteinases, cyclooxygenase 2 (COX -2), inducible nitric oxide synthase (iNOS). In the meantime, Nrf2-mediated downstream genes with cytoprotective capacity are involved in the regulation of the innate immune response while inhibiting the expression of proinflammatory genes. This review highlights the protective role of Nrf2 in inflammation-related diseases, focusing on the regulation of inflammatory signals by this transcription factor.