Itami T, Kanoh S
Jpn J Pharmacol. 1983 Dec;33(6):1199-204. doi: 10.1254/jjp.33.1199.
Our previous paper reported that the fetotoxic effects of aspirin (ASA) were enhanced by bacterial endotoxin (LPS), and the effects of ASA were attributed to its major metabolite, salicylic acid (SA), as indicated by high SA concentrations in fetus and placenta. In order to clarify the mechanisms of the enhancement by LPS, serum total protein, albumin and free fatty acid (FFA) levels and SA-binding capacity of serum protein were investigated in pregnant rats. The following results were obtained: 1) FFA levels increased steadily after day 16 of pregnancy, and SA-binding capacity of serum protein decreased gradually after day 18, as the pregnancy proceeded to full term. 2) LPS injection decreased total protein and albumin levels in normal and starved rats on day 15 of pregnancy. 3) Starvation and/or LPS injection potentiated the increase of FFA level and reduced significantly SA-binding capacity of serum protein in the rats on day 15 of pregnancy. 4) Serum protein showing low SA-binding capacity from LPS-treated rats recovered normal SA-binding capacity when FFA was removed from serum protein by charcoal treatment. These data suggested the decrease of the SA-protein binding in serum by the increased level of FFA, an inhibitor of the binding, and the decreased level of albumin as a possible mechanism for the potentiation of the fetotoxicities of ASA by LPS.
我们之前的论文报道,细菌内毒素(LPS)可增强阿司匹林(ASA)的胚胎毒性作用,且ASA的作用归因于其主要代谢产物水杨酸(SA),胎儿和胎盘中SA的高浓度表明了这一点。为了阐明LPS增强作用的机制,我们对妊娠大鼠的血清总蛋白、白蛋白和游离脂肪酸(FFA)水平以及血清蛋白的SA结合能力进行了研究。得到了以下结果:1)妊娠第16天之后FFA水平稳步升高,随着妊娠进展至足月,血清蛋白的SA结合能力在第18天之后逐渐降低。2)在妊娠第15天,LPS注射降低了正常和饥饿大鼠的总蛋白和白蛋白水平。3)饥饿和/或LPS注射增强了妊娠第15天大鼠FFA水平的升高,并显著降低了血清蛋白的SA结合能力。4)当通过活性炭处理从血清蛋白中去除FFA时,LPS处理大鼠中SA结合能力低的血清蛋白恢复了正常的SA结合能力。这些数据表明,作为结合抑制剂的FFA水平升高以及白蛋白水平降低导致血清中SA - 蛋白结合减少,这可能是LPS增强ASA胚胎毒性的机制。