乙酰化鞘磷脂的paf样活性。

Biomedical science Pub Date : 1991-01-01
E V Berdyshev, O E Getmanova
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引用次数: 0

摘要

在体外实验中发现o -乙酰化鞘磷脂(Ac-SM)可引起兔血小板聚集。ac - sm诱导的聚集伴随着血小板对血小板活化因子(PAF)的脱敏。Ac-SM的活性约为酰基- paf的4倍。BN 52021是一种特异性的paf受体拮抗剂,被发现可以抑制ac - sm诱导的聚集。这些结果,连同先前关于鞘磷脂可以抑制PAF作用的报道,提示鞘磷脂作为PAF受体结合的调节剂具有新的生理功能。为了证实鞘磷脂衍生物的生理存在,需要寻找特异性催化鞘磷脂乙酰化和去乙酰化的酶。
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PAF-like activity of O-acetylated sphingomyelin.

O-acetylated sphingomyelin (Ac-SM) was found to cause aggregation of rabbit platelets in vitro. The Ac-SM-induced aggregation was accompanied by subsequent desensitisation of platelets to platelet-activating factor (PAF). The activity of Ac-SM exceeded that of acyl-PAF by about fourfold. BN 52021, a specific PAF-receptor antagonist, was found to inhibit the Ac-SM-induced aggregation. These results, together with earlier reports that sphingomyelin can inhibit the effects of PAF, suggest a new physiological function for sphingomyelin as a regulator of PAF-receptor binding. A search for enzymes to catalyse specifically the acetylation and deacetylation of sphingomyelin is required to confirm the physiological existence of sphingomyelin derivatives.

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