首页> 美国卫生研究院文献>Annals of the Rheumatic Diseases >Studies on the mechanism of inhibition of chemotactic tripeptide stimulated human neutrophil polymorphonuclear leucocyte superoxide production by chloroquine and hydroxychloroquine.
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Studies on the mechanism of inhibition of chemotactic tripeptide stimulated human neutrophil polymorphonuclear leucocyte superoxide production by chloroquine and hydroxychloroquine.

机译:氯喹和羟氯喹抑制趋化三肽刺激人嗜中性粒细胞多形核白细胞产生过氧化物的机理研究。

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摘要

The effect of chloroquine and hydroxychloroquine on neutrophil superoxide release stimulated by the chemotactic tripeptide N-formyl-methionyl-leucyl-phenylalanine (FMLP) was examined. Both drugs caused time and dose dependent inhibition of superoxide release but had no effect on equilibrium binding of [3H]FMLP to its receptor. Preliminary experiments suggest that these drugs may exert their inhibitory effect on superoxide release by inhibiting the FMLP stimulated hydrolysis of phosphoinositides.
机译:研究了氯喹和羟氯喹对趋化三肽N-甲酰基-甲硫酰基-亮氨酰-苯丙氨酸(FMLP)刺激的嗜中性白细胞超氧化物释放的影响。两种药物均引起时间和剂量依赖性的超氧化物释放抑制,但对[3H] FMLP与其受体的平衡结合没有影响。初步实验表明,这些药物可能通过抑制FMLP刺激的磷酸肌醇水解而发挥其对超氧化物释放的抑制作用。

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