低密度脂蛋白对人血小板磷脂酰肌醇代谢产物及钙摄取的影响

观察了低密度脂蛋白(LDL)或高密度脂蛋白(HDL)加LDL对人血小板磷脂酰肌醇循环中的重要物质磷脂酰肌醇4,5-二磷酸(PIP_2),磷脂酸(PA),以及~(45)Ca~(2+)摄取的影响,同时还观察了LDL,HDL对猪肺微粒体酶催化前列腺素内过氧化物生成血栓素B_2(TXB_2)的影响.结果表明,LDL引起血小板PIP_2短暂下降,继之增加,同时伴有PA的增加,未观察到HDL拮抗LDL的作用,此外,LDL能刺激Ca~(2+)内流入血小板.HDL明显抑制TXB_2生成。

Effect of low density lipoproteins on the metabolites of phospha-tidylinositol and calcium uptake in human platelets

Low density lipoproteins(LDL)and high density lipoproteins(HDL)were separated from normal human serum.The effects of LDL or HDL plus LDL on changes of phosphatidylinositol 4.5 bisphosphate(PIP2)and phosphatidic acid(PA)in 32P labelled isolated human platelets as well as 45Ca2+ uptake by Quin2(a fluorescent indicator)loaded platelets were studied.In addition,using prostaglandin endoperoxide as substrate and pig lung microsomes as enzyme source,the effect of LDL or HDL on thromboxane B2(TXB2)generation was determined by RIA.The results indicate that LDL causes a transient decline of PIP2 level within 15 s followed by a significant increase.This was accompanied simul taneously by a gradual increase of PA level for 60 s.The effects of LDL on PIP2 and PA are dosedependent.However.HDL does not show any antagonized effect of LDL on PIP,and PA.In addition.LDL was found to stimulate 45Ca2+ uptake by human platelets.Furthermore,after loading of platelets with the fluorescent probe Quin2.the uptake of 45Ca2+ by loaded platelets was much more than that by unloaded platelets,suggesting that LDL induces a Ca2+ influx.With prostaglandin endoperoxide as substrate.LDL had no effect on TXB2 generation whereas HDL inhibited TXB2 production in a dose dependent manner.