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）、一氧化氮（NO）释放和脂质过氧化的产生和活性，雌激素受体α（ER-α）的表达与细胞因子的作用密切相关，联合应用细胞因子和雌激素对高ER-α的乳腺癌有明显的治疗作用。α表达的成纤维细胞减少了细胞内ROS和NO的产生，脂质过氧化产物的产生，并随后阻止了凋亡性细胞死亡，尽管低表达的ER-结果表明，雌激素对α细胞的损伤起重要的保护作用，苦参碱通过控制NO和ROS的产生和脂质过氧化作用诱导细胞死亡。

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.