Zinchenko V P, Mysiakin E B, Dolgachev V A, Dedkova E N, Safronova V G, Gapeev A B, Shebzukhov Iu V, Vaĭsbud M Iu
Biofizika. 1997 Sep-Oct;42(5):1097-105.
Direct and modulate effects of platelet activating factor (PAF), its structural analogues and ATP on primary and second processes at peritoneal neutrophils and P388D1 cells activation has been studied. The effect of compounds was evaluated on changes in Ca2+ transport and generation of reactive oxygen species. It was shown, that the synthetic analogues of MS series interact with PAF receptor, mobilize Ca2+ from thapsigargin-dependent intracellular stores and inhibit Ca2+ response on PAF in both types of cells. Unlike PAF the analogues do not induce the formations of reactive oxygen species in neutrophils and inhibit the PMA-induced respiratory burst. The activation of pyrinoreceptor of P388D1 cells by exogenous ATP does not inhibit PAF induced Ca2+ rise in cytoplasm, though partly releases Ca2+ from the same store.
研究了血小板活化因子(PAF)、其结构类似物和ATP对腹膜中性粒细胞和P388D1细胞活化的初级和次级过程的直接和调节作用。评估了化合物对Ca2+转运变化和活性氧生成的影响。结果表明,MS系列合成类似物与PAF受体相互作用,从毒胡萝卜素依赖的细胞内储存中动员Ca2+,并抑制两种类型细胞中PAF引起的Ca2+反应。与PAF不同,这些类似物不会在中性粒细胞中诱导活性氧的形成,并抑制佛波酯诱导的呼吸爆发。外源性ATP对P388D1细胞的嘧啶受体的激活不会抑制PAF诱导的细胞质Ca2+升高,尽管它会部分地从同一储存中释放Ca2+。