Liu W K, Tsui K W, Wong C C
Department of Anatomy, Faculty of Medicine, Chinese University of Hong Kong, Shatin, N.T.
Virchows Arch B Cell Pathol Incl Mol Pathol. 1993;63(2):131-6. doi: 10.1007/BF02899252.
In this study we compared the functions of normal peritoneal macrophages with those from methimazole-induced hypothyroid C57BL/6 mice. Methimazole (MMI) suppressed the expression of the tumor necrosis factor (TNF) gene in peritoneal macrophages (MAM) at both transcriptional and translational levels. The kinetics of TNF synthesis by MAM following in vivo and in vitro lipopolysaccharide (LPS) challenge were different, but both treatments resulted in significant decreases (P < 0.05) in TNF mRNA and protein after 60 min. Similarly, the production of reactive nitrogen and oxygen intermediates by MAM were significantly (P < 0.05) lower compared with control macrophages (CAM). In addition, the serum TNF protein was significantly lower (P < 0.05) in MMI-treated mice following intravenous LPS challenge for 90 min. These data suggested that peritoneal macrophages were inactivated in MMI-induced hypothyroid mice.
在本研究中，我们比较了正常腹膜巨噬细胞与来自甲巯咪唑诱导的甲状腺功能减退C57BL/6小鼠的腹膜巨噬细胞的功能。甲巯咪唑（MMI）在转录和翻译水平均抑制腹膜巨噬细胞（MAM）中肿瘤坏死因子（TNF）基因的表达。体内和体外脂多糖（LPS）刺激后，MAM合成TNF的动力学不同，但两种处理在60分钟后均导致TNF mRNA和蛋白显著降低（P < 0.05）。同样，与对照巨噬细胞（CAM）相比，MAM产生的活性氮和氧中间体显著（P < 0.05）降低。此外，静脉注射LPS 90分钟后，MMI处理的小鼠血清TNF蛋白显著降低（P < 0.05）。这些数据表明，在MMI诱导的甲状腺功能减退小鼠中，腹膜巨噬细胞被灭活。
