Analysis for Estrogen Receptors Detected on the Rheumatoid Arthritis Synovial Cells by Immunofluorescent Bioimaging

免疫荧光生物成像分析类风湿性关节炎滑膜细胞上的雌激素受体

• 批准号: 14571796
• 负责人: SUENAGA Shigeaki
• 金额: $ 1.92万
• 依托单位: Kagoshima University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 2002
• 资助国家: 日本
• 起止时间: 2002 至 2003
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-14571796/
• 关键词: Rheumatoid arthritis; Estrogen; Estrogen receptor; Reactive oxygen species; NO; Lipid peroxidation; Apoptosis; iNOS mRNA; NOS mRNA; 慢性リウマチ性関節炎; 蛍光バイオイメージング法

The aim of this investigation was to hypothesize that 17β-estradiol(estrogen)can modulate the production and activity of reactive oxygen species(ROS), nitric pxide(NO)synthasis, and lipid peroxidation in fibroblast-like synovial cells, and the effects are dependent on the expressions of estrogen receptor alpha(ER-α).The results showed that the combined treatment of cytokines and estrogen for the high ER-α expressed fibroblasts decreased the intracellular ROS and NO generation, lipid peroxidation production and subsequent prevented apoptotic cell death, although the low expressed ER-α cells did not show the substantial change.The experiments on levels of iNOS mRNA confirmed the NO levels.These results suggest that estrogen plays an important role in protecting cells against cytokine-induced cell death by controlling the generation of NO and ROS and lipid peroxidation.

为探讨17β-雌二醇(雌激素)对成纤维细胞样滑膜细胞内活性氧(ROS)、一氧化氮(NO)合成和脂质过氧化的调节作用，其作用依赖于雌激素受体α(ER-α)的表达。结果表明，细胞因子和雌激素联合作用可减少ER-α高表达的成纤维细胞内ROS和NO的生成、脂质过氧化产物的产生，从而阻止细胞死亡。虽然低表达的ER-α细胞没有表现出实质性的变化。iNOS mRNA水平的实验证实了NO的水平。这些结果表明，雌激素通过控制NO和ROS的产生以及脂质过氧化，在保护细胞免受细胞因子诱导的细胞死亡方面发挥了重要作用。