A study on altered immune function in rheumatoid arthritis through disfunction of transcription factor

已知NF-KB在巨噬细胞的调控中起重要作用。部分受氧化还原机制调控。在本研究中，抗风湿药物、d -青霉胺、布西拉胺、auranofine增加THP-1细胞内活性氧的数量，并下调其增殖。提示这些药物通过增加活性氧来抑制NF-KB的活性。研究了细胞内活性氧增加诱导细胞凋亡的可能性。buillamine首先诱导活性氧的产生和THP-1细胞膜通透性的改变。结果THP-1出现凋亡。提示buillamine通过诱导细胞凋亡抑制类风湿关节炎滑膜细胞的增殖。

NF-KB is known to play a important role in the regulation of macrophages. It is partially regulated by redox mechanism. In this study, anti-rheumatic drugs, D-penicillamine, bucillamine, auranofine increased the amount of intracellular reactive oxygen species of THP-1, moreover, downregulated their proliferation. It was suggested that these drugs suppressed the activity of NF-KB through the increase of reactive oxygen species.Possibility of the apoptosis induction through the increase of intracelllar reactive oxygen species was also studied. Bucillamine first induced the production of reactive oxygen species and the change of membrane permeability of THP-1. Consequently, apoptosis of THP-1 turned out. It was suggested that bucillamine suppressed the proliferation of synovial cells in rheumatoid arthritis through the induction of apoptosis.