MAPKs与Keap1-Nrf2-ARE信号通路的窜扰作用在慢性阻塞性肺疾病中的作用及意义  

Roles of the cross talk between MAP kinases and Keap1-Nrf2-ARE signaling pathways in chronic obstructive pulmonary disease

作　　者：王淑君[1] 陈亚军[1] 汪珊珊[1] 汪电雷[1,2] 汪辰吟[1] 杨丽丽[1] 陈金佩[1] 

机构地区：[1]安徽中医药大学药学院,安徽合肥230031 [2]f安徽中医药大学药物代谢动力学研究室,安徽合肥230031

出　　处：《药学学报》2015年第2期133-140,共8页Acta Pharmaceutica Sinica

基　　金：国家自然科学基金资助项目(81001592,81473536)

摘　　要：慢性阻塞性肺疾病(chronic obstructive pulmonary disease,COPD)是一种可预防和治疗的疾病,与有害颗粒或气体对肺损伤有关,病理特征为气流受限、慢性呼吸道炎症,其主要病理表现为炎症反应、黏液分泌过量、氧化应激和上皮细胞凋亡。现代研究表明,MAPKs与Keap1-Nrf2-ARE信号通路参与调控炎症、氧化应激等病理过程。本文重点探讨以上信号通路在炎症反应、黏液分泌过量、氧化应激和上皮细胞凋亡中的相互影响,并在此基础上关注与MAPKs及Keap1-Nrf2-ARE信号通路相关的药物,以期阐明MAPKs和Keap1-Nrf2-ARE信号通路及其窜扰作用在调控COPD病理生理中的重要作用和意义,同时为COPD防治的药物研究和开发提供更多思路。Chronic obstructive pulmonary disease（COPD）, a common preventable and treatable disease, is characterized by airflow limitation that is usually progressive and associated with an enhanced chronic inflammatory response in the airways. Its main pathological manifestations include airway inflammation, mucus hypersecretion, oxidative stress and apoptotic epithelial cells. Recent research suggests that MAP kinases and Keap1-Nrf2-ARE signaling pathway are involved in the pathological process of inflammation and oxidative stress. This review explores the potential role of the cross talk of these signaling pathways in airway inflammation, mucus hypersecretion, oxidative stress and apoptotic epithelial cells. To clarify the roles of cross talk between MAP kinases and Keap1-Nrf2-ARE signaling pathway, we also focus on the drugs related to that in the treatment of COPD, and it provides ideas for more drug research in the treatment of COPD.

关 键 词：慢性阻塞性肺疾病 有丝分裂素激活蛋白激酶类 核因子E2相关因子2 

分 类 号：R34[医药卫生—基础医学] R963