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紫杉醇可抑制N-甲酰甲硫氨酰-亮氨酰-苯丙氨酸(FMLP)诱导的人中性粒细胞极化和过氧化氢生成,同时降低[3H]FMLP结合。

Taxol inhibits N-formyl-methionyl-leucyl-phenylalanine (FMLP)-induced human neutrophil polarization and H2O2 production while decreasing [3H]FMLP binding.

作者信息

Iannone M A, Wolberg G, Reynolds-Vaughn R, Zimmerman T P

机构信息

Wellcome Research Laboratories, Research Triangle Park, NC 27709.

出版信息

Agents Actions. 1987 Aug;21(3-4):278-80. doi: 10.1007/BF01966490.

Abstract

We have studied the effect of taxol on two N-formyl-methionyl-leucyl-phenylalanine (FMLP)-induced neutrophil functions and the possible mechanism by which it inhibits these functions. Taxol inhibited FMLP-induced human neutrophil polarization (a characteristic change in neutrophil shape in response to a chemotactic stimulus) and H2O2 generation. Taxol also decreased the specific binding of [3H]FMLP to human neutrophils at 4 degrees C. The decreased binding of FMLP to its receptor may be responsible for the inhibition by taxol of FMLP-induced polarization and H2O2 generation.

摘要

我们研究了紫杉醇对两种N-甲酰甲硫氨酰-亮氨酰-苯丙氨酸(FMLP)诱导的中性粒细胞功能的影响及其抑制这些功能的可能机制。紫杉醇抑制了FMLP诱导的人类中性粒细胞极化(中性粒细胞形状响应趋化刺激的特征性变化)和H2O2生成。紫杉醇还降低了4℃时[3H]FMLP与人中性粒细胞的特异性结合。FMLP与其受体结合的减少可能是紫杉醇抑制FMLP诱导的极化和H2O2生成的原因。

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