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

本研究的目的是假设17β-雌二醇（雌激素）可以调节成纤维细胞样滑膜细胞中活性氧（ROS）的产生和活性、一氧化氮（NO）的合成和脂质过氧化，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处理高ER-α表达的成纤维细胞，可减少细胞内ROS和NO的生成、脂质过氧化的产生，从而防止凋亡细胞死亡，而低ER-α表达的成纤维细胞则无明显变化。iNOS mRNA水平实验证实了NO水平。这些结果表明，雌激素通过控制NO和ROS的生成以及脂质过氧化作用，在保护细胞免受细胞因子诱导的细胞死亡中起重要作用。

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.