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首页> 外文期刊>Life sciences >PGI(2) ANALOGUE, SODIUM BERAPROST, SUPPRESSES SUPEROXIDE GENERATION IN HUMAN NEUTROPHILS BY INHIBITING P47PHOX PHOSPHORYLATION
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PGI(2) ANALOGUE, SODIUM BERAPROST, SUPPRESSES SUPEROXIDE GENERATION IN HUMAN NEUTROPHILS BY INHIBITING P47PHOX PHOSPHORYLATION

机译：PGI（2）模拟物贝拉前列素通过抑制P47PHOX磷酸化抑制人中性粒细胞中过氧化物的生成

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Sodium beraprost, a newly synthesized PGl(2) analogue inhibited in a dose-dependent manner formyl-methionyl-leucyl-phenylalanine (fMLP) induced superoxide generation of human neutrophils, but it had no effect on the superoxide synthesis by phorbol myristate acetate (PMA) or A23187. Sodium beraprost inhibited Ca2+ influx in fMLP stimulated neutrophils employing fluorometry and confocal microscopy. These findings suggested that the inhibitory effect of sodium beraprost on fMLP induced speroxide generation was due to suppression of Ca2+ influx. To examine the relationship between the effect of sodium beraprost and phosphorylation of p47phox (the 47kDa cytosolic phagocyte oxidase factor), immuno-precipitation of p47phox and western blotting for phospho-amino acids were performed. Phosphorylation of serine residues of p47phox induced by fMLP was reduced in the presence of sodium beraprost in a dose-dependent manner. The reduction in phosphorylation was accompanied by a reduction in p47phox and p67phox translocation to the plasma membrane and superoxide generation. These findings suggested that p47phox phosphorylation was necessary for translocation and superoxide generation in fMLP activated neutrophils, and that p47phox phosphorylation was regulated by a Ca2+ dependent mechanism. These observations suggested that sodium beraprost inhibited fMLP induced superoxide generation of human neutrophils by the inhibition of p47phox phosphorylation and translocation by a Ca2+ dependent mechanism. [References: 33]
机译：贝拉前列素钠，一种新合成的PGl（2）类似物，以剂量依赖的方式抑制甲酰基-蛋氨酸-亮氨酰-苯丙氨酸（fMLP）诱导人类中性粒细胞的超氧化物生成，但对佛波肉豆蔻酸酯乙酸盐（PMA）的超氧化物合成没有影响）或A23187。使用荧光测定法和共聚焦显微镜，贝拉前列素钠可抑制fMLP刺激的中性粒细胞中的Ca2 +流入。这些发现表明贝拉前列素钠对fMLP诱导的过氧化物生成的抑制作用是由于抑制Ca2 +流入。为了检查贝拉前列素钠的作用与p47phox（47kDa胞质吞噬细胞氧化酶因子）磷酸化之间的关系，进行了p47phox的免疫沉淀和磷酸化氨基酸的蛋白质印迹。在贝拉前列素钠存在下，由fMLP诱导的p47phox丝氨酸残基的磷酸化作用呈剂量依赖性。磷酸化的减少伴随着p47phox和p67phox向质膜的易位减少以及超氧化物的产生。这些发现表明，p47phox磷酸化对于fMLP激活的中性粒细胞的转运和超氧化物生成是必需的，并且p47phox磷酸化受Ca2 +依赖性机制调节。这些观察结果表明贝拉前列素钠通过抑制Ca2 +依赖性机制抑制p47phox磷酸化和易位而抑制了fMLP诱导的人类嗜中性粒细胞超氧化物生成。 [参考：33]

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