Sipe J D
Br J Exp Pathol. 1978 Jun;59(3):305-10.
SAA is a normal acute-phase serum protein which has been identified by its cross-reaction with antibodies to the amyloid A fibril protein, AA, that is associated with secondary amyloidosis. The induction of SAA by bacterial lipopolysaccharide (LPS) has been studied with 3 inhibitors of protein synthesis: cycloheximide, actinomycin D, and galactosamine. Each of the 3 agents when administered simultaneously with LPS completely abolishes induction of SAA for at least 6 h. They are all significantly effective when given 1.5 h after LPS but 3 h after LPS the inhibitory effect of actinomycin D on SAA induction is markedly reduced. Cycloheximide alone can also induce significant concentration of SAA, but a longer time is required than for LPS. Thus it appears that the acute-phase SAA response is characterized by both RNA and protein synthesis which is initiated by the acute-phase inducing agent and which precedes the appearance of elevated SAA concentrations in the serum.
血清淀粉样蛋白A(SAA)是一种正常的急性期血清蛋白,它通过与抗淀粉样蛋白A(AA)纤维蛋白抗体的交叉反应而被识别,AA与继发性淀粉样变性有关。已经用三种蛋白质合成抑制剂研究了细菌脂多糖(LPS)对SAA的诱导作用:环己酰亚胺、放线菌素D和半乳糖胺。这三种药物中的每一种与LPS同时给药时,至少6小时内完全消除SAA的诱导。它们在LPS给药后1.5小时给药时都有显著效果,但在LPS给药后3小时,放线菌素D对SAA诱导的抑制作用明显降低。单独使用环己酰亚胺也能诱导SAA达到显著浓度,但所需时间比LPS诱导的时间长。因此,似乎急性期SAA反应的特征是RNA和蛋白质合成,这是由急性期诱导剂启动的,并且在血清中SAA浓度升高之前出现。