Nrf2活化下调AGEs诱导的内皮细胞活性氧水平  

Activation of Nrf2 decreased reactive oxygen species in endothelial cells stimulated by advanced glycation end products

作　　者：刘洪彬 于世勇[2] 

机构地区：[1]重庆市九龙坡区第五人民医院内科,401329 [2]第三军医大学新桥医院心内科,重庆400037

出　　处：《重庆医学》2011年第33期3329-3330,3334,共3页Chongqing medicine

基　　金：国家自然科学基金资助项目(81000134)

摘　　要：目的探讨激活红系衍生的核因子2相关因子2(Nrf2)对晚期糖基化终末产物(AGEs)作用下的内皮细胞内活性氧(ROS)水平的影响。方法培养人脐静脉内皮细胞(HUVECs),通过Nrf2激动剂莱菔硫烷(SFN)激活Nrf2,观察AGEs刺激下HUVECs细胞ROS生成情况。结果 Nrf2活化可显著降低AGEs刺激后内皮细胞ROS水平(P<0.05)。结论增强Nrf2信号通路活性,能起到拮抗AGEs诱导内皮细胞氧化损伤的作用,从而为动脉粥样硬化尤其是糖尿病心血管并发症的防治提供新的思路和靶点。Objective To investigated the role of Nrf2 activation in the generation of intracellular ROS in endothelial cells stimu- lated by AGEs. Methods Human umbilical vein endothelial cells（HUVECs） were cultured and incubated with AGEs and intracel- lular ROS was measured with 2＇, 7＇-dichlorodihydrofluorescein diacetate（DCF DA）. Sulforaphane was used to activate Nrf2. The role of Nrf2 in the generation of ROS was observed. Results Nrf2 activation inhibited the generation of intracellular ROS signifi cantly（P〈0.05）. Conclusion Enhancement of Nrf2 pathway can reduce the AGEs-induced oxidative injury of endothelial cells,and indicate a potential target for the inhibition of the atherogenic signals triggered by AGEs.

关 键 词：内皮细胞 活性氧 红系衍生的核因子2相关因子2 晚期糖基化终末产物 

分 类 号：R587.2[医药卫生—内分泌]