姜黄素
Notch信号通路
氧化应激
赫斯1
细胞生物学
化学
信号转导
活性氧
人脐静脉内皮细胞
活力测定
细胞凋亡
脐静脉
药理学
生物
生物化学
体外
作者
Yang Yang,Weixun Duan,Zhenxin Liang,Wei Yi,Juanjuan Yan,Ning Wang,Yue Li,Wensheng Chen,Shiqiang Yu,Zhenxiao Jin,Dinghua Yi
标识
DOI:10.1016/j.cellsig.2012.11.025
摘要
Previous studies have demonstrated that Notch signaling pathway plays a regulatory role in cellular oxidative stress injury (OSI). In this study, our aim was to explore the role of the Notch signaling pathway in hydrogen peroxide (H2O2)-induced OSI and the protective effect of curcumin during (H2O2)-induced injury in human umbilical vein endothelial cells (HUVECs). DAPT, a specific inhibitor of the Notch signaling pathway, and Notch1 siRNA were used to study Notch activity. Further, HUVECs were exposed to H2O2 in the absence or presence of curcumin. DAPT and Notch1 siRNA significantly inhibited OSI and the expression of Notch1 and Hes1. Curcumin conferred a protective effect on the HUVECs against H2O2, which was evidenced by improved cell viability, adhesive ability and migratory ability and a decreased apoptotic index, decreased production of reactive oxygen species (ROS) and a reduction in several biochemical parameters. Immunofluorescence and Western blotting analyses demonstrated that H2O2 treatment upregulated the expression of Notch1, Hes1, Caspase3, Bax and cytochrome c downregulated the expression of Bcl2, and treatment with curcumin reversed these effects. We demonstrated for the first time that the inhibition of Notch signaling pathway imparts a protective effect against endothelial OSI. The protective effects of curcumin against OSI are at least in part dependent on Notch1 inhibition.
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