中国体外循环杂志2019，Vol.17Issue(1)：41-47,7.DOI:10.13498/j.cnki.chin.j.ecc.2019.01.10
黄连素激活核因子E2相关因子/血红素氧合酶-1增强内皮细胞抗过氧化氢损伤
Protective effects of Berberine on H2O2-induced endothelial cell death through Nrf2/HO-1 pathway
摘要
Abstract
Objective To investigate whether berberine (BBR) could protect human umbilical vein endothelial cells (HUVECs) against H2O2-induced injury by activating nuclear factor erythroid 2-related factor 2/heme oxygenase-1 (Nrf2/HO-1) signaling pathway. Methods After pretreated with BBR (5 and 10 μmol/L) for 12 h, HUVECs cells were then insulted by H2O2 (200μmol/L) for additional 4 h. The cell viability was evaluated by CCK-8 analysis. The apoptotic cells were measured with TUNEL stainning. The cellular reactive oxygen species (ROS) was detected by DCFH-DA. The distribution of Nrf2 in cells was marked by immunofluorescence. Western blotting was used to analyze the proteins expression of Nrf2/HO-1 signaling pathway. Additionally, the detections above were repeated after Nrf2 siRNA treatment. Results Compared with control group, H2O2 decreased cell activity and increased apoptosis and ROS levels in HUVECs (P ＜0.05). Different concentrations of BBR (5 and 10 μmol/L) effectively inhibited the changes above in a dose-dependent manner (P ＜ 0.05). Meanwhile, BBR further enhanced the translocation of Nrf2 from cytoplasm to nucleus and the expression of HO-1, which was induced by H2O2 injury (P ＜0.05). Nrf2 siRNA not only significantly inhibited the activation of Nrf2/HO-1, but also obviously reversed the protective effects of BBR on HUVECs (P ＜ 0.05). Conclusion BBR promotes the ability of HUVECs to scavenge ROS by activating the Nrf2/HO-1 pathway in H2O2-induced injury.关键词
黄连素/核因子E2相关因子/血红素氧合酶-1/人脐静脉内皮细胞/活性氧/凋亡Key words
Berberine/Nuclear factor erythroid 2-related factor 2/heme oxygenase-1/Human umbilical vein endothelial cell/Reactive oxygen species/Apoptosis引用本文复制引用
王臻,丁慧,杨瑞..黄连素激活核因子E2相关因子/血红素氧合酶-1增强内皮细胞抗过氧化氢损伤[J].中国体外循环杂志,2019,17(1):41-47,7.基金项目
陕西省科技研究发展计划 (2012K13-02-23) （2012K13-02-23）
