Brandwein S R, Sipe J D, Tatsuta E, Skinner M, Cohen A S
J Rheumatol. 1984 Oct;11(5):597-601.
The effects of colchicine on the acute phase serum amyloid A (SAA) response were studied in CBA/J mice to determine whether these effects are mediated via inhibition of interleukin-1 (IL-1) production. Prolonged pretreatment (72 h) with colchicine blunted the SAA response to stimulation with silver nitrate (AgNO3), while brief pretreatment (12 h) unexpected augmented SAA production. In a macrophage model, colchicine stimulated baseline production of IL-1 (SAA inducer and lymphocyte activating factor activities) and augmented lipopolysaccharide (LPS) induced IL-1 production. This indicates that colchicine does not inhibit amyloidosis via direct effects on early inducers of the acute phase SAA response.
在CBA/J小鼠中研究了秋水仙碱对急性期血清淀粉样蛋白A（SAA）反应的影响，以确定这些影响是否通过抑制白细胞介素-1（IL-1）的产生介导。用秋水仙碱进行长时间预处理（72小时）可减弱SAA对硝酸银（AgNO3）刺激的反应，而短暂预处理（12小时）意外地增加了SAA的产生。在巨噬细胞模型中，秋水仙碱刺激了IL-1的基础产生（SAA诱导剂和淋巴细胞激活因子活性），并增强了脂多糖（LPS）诱导的IL-1产生。这表明秋水仙碱不是通过对急性期SAA反应的早期诱导剂的直接作用来抑制淀粉样变性。
