Hänsch G M, Gemsa D, Resch K
J Immunol. 1985 Aug;135(2):1320-4.
Treatment of human platelets by the purified late complement components C5b-9 results in a dose- and time-dependent release of prostaglandin E (PGE) and thromboxane B2 (TXB2). To study the mechanism underlying the complement-induced prostanoid synthesis, we examined whether C5b-9 affected the enzyme acyl-coA:lysolecithin acyltransferase (E.C.2.3.1.2.3) that catalyzes the reinsertion of liberated arachidonic acid, the precursor molecule of the prostanoids. With C5b-9 doses sufficient to induce prostanoid synthesis, the activity of lysolecithin acyltransferase, measured as conversion of lysophosphatidyl choline to phosphatidyl choline, was inhibited. For comparison, another channel-forming substance, nystatin, was studied. Nystatin had an effect similar to C5b-9: PGE and TXB2 release was stimulated, whereas acyltransferase activity was inhibited. These finding support the concept that inhibition of lysolecithin acyltransferase might be the prerequisite for prostanoid production.
用纯化的补体晚期成分C5b - 9处理人血小板，会导致前列腺素E（PGE）和血栓素B2（TXB2）呈剂量和时间依赖性释放。为了研究补体诱导前列腺素合成的潜在机制，我们检测了C5b - 9是否影响催化游离花生四烯酸（前列腺素的前体分子）重新插入的酶酰基辅酶A：溶血卵磷脂酰基转移酶（E.C.2.3.1.2.3）。在足以诱导前列腺素合成的C5b - 9剂量下，以溶血磷脂酰胆碱转化为磷脂酰胆碱来衡量的溶血卵磷脂酰基转移酶活性受到抑制。作为比较，研究了另一种形成通道的物质制霉菌素。制霉菌素具有与C5b - 9类似的作用：刺激PGE和TXB2释放，而抑制酰基转移酶活性。这些发现支持这样一种概念，即抑制溶血卵磷脂酰基转移酶可能是前列腺素产生的前提条件。
