The role of reactive oxygen species (ROS) in the progressive kidney disease in children, and therapeutic strategy based on its mechanisms.

研究了活性氧在肾小球肾炎（GN）细胞表型改变中的作用。在GN新月体中观察到ROS产生增加。增加的ROS产生与增强的Nox 2（NADPH组分）表达和壁上皮细胞增殖相关。同时观察血管紧张素II及其受体的表达。此外，培养的肾小球细胞刺激血管紧张素II和H2 O2显示增强的磷酸化Erk 5，ROS相关的MAPK家族。siRNA抑制表明ROS-MAP激酶信号通路可能增强细胞的生存能力，从而在肾小球肾炎的进展中发挥作用。

The role of reactive oxygen species for cell phenotypic changes was investigated in glomerulonephritis (GN). Increased ROS production was observed in crescents of GN. The increased ROS production was associated with enhanced Nox2 (an NADPH component) expression and parietal epithelial cell proliferation. We also observed the expressions of angiotensin II and its receptor. In addition, cultured glomerular cells stimulated with angiotensin II and H2O2 showed the enhanced phosphorylation of Erk5, a ROS-related MAPK family. Inhibition with siRNA showed that ROS-MAP kinase signaling pathway might enhance cell potential to survive, and thereby play a role in progression of glomerulonephritis.