FMLP刺激HL-60细胞NADPH氧化酶激活的信号转导途径  

Signaling pathways of activation of NADPH oxidase in HL-60 cells wi th fMLP stimulation

作　　者：崔玉东[1] 稻波修[2] 山盛■ 桑原干典 

机构地区：[1]黑龙江八一农垦大学基因工程中心,黑龙江密山158308 [2]北海道大学兽医学部放射生物学实验室

出　　处：《免疫学杂志》2001年第5期359-363,共5页Immunological Journal

摘　　要：目的澄清中性粒细胞中 [Ca2 + ]i 及某些激酶在 NADPH氧化酶激活中的作用和 NADPH氧化酶激活的信号转导途径。方法利用中性粒细胞样 HL- 60细胞 ,研究 [Ca2 + ]i 和某些激酶对 f ML P刺激 NADPH氧化酶激活的影响。结果用 10μm ol/ L BAPTA- AM去除 [Ca2 + ]i 后使 O- 2 生成明显减少 ;8μm ol/ L的 PKC抑制物 GF10 92 0 3 x显著地抑制了 O- 2 产生 ;5 0 μmol/ L 的 p3 8抑制物 SB2 0 3 5 80、5 0 μm ol/ L 的 ERK抑制物 PD0 980 5 9和 0 .1μm ol/ L 的 PI3K抑制物 Wortm annin使O- 2 产生受到不同程度抑制 ;PKC、PI3K、p3 8和 ERK激活对 [Ca2 + ]i 升高没有影响 ;[Ca2 + ]i、PKC和 PI3 K对 p3 8激活有一定作用 ,而 ERK和 Akt激活主要受 PI3- K的调控。结论试验说明 [Ca2 + ]i 依赖途径 ( PKC)和 [Ca2 + ]i 非依赖途径 ( PI3K、p3 8和ERK)对ObjectiveTo investigate the effects of intracellular Ca 2+ ([Ca 2+ ] i) and kinases on the activation of NADPH oxida se and the signaling pathways of activation of NADPH oxidase in neutr ophils Methods The influence of [Ca 2+ ] i and some kinases on the activation of NADPH oxidase were studied in differentiated HL 6 0 with fMLP stimulation Results 1 0 μmol/L BAPTA AM significantly attenuated the fMLP induced O - 2 generation 8 μmol/L GF10929 3x remarkably inhibited O - 2 generation 50 μmol/L SB20358 0, 50 μmol/L PD98059 and 0 1 μmol/L wortmannin suppress ed O - 2generation in some degree The activation of PKC, PI 3K , p38 and ERK was not essential to [Ca 2+ ] i elevation C er tain effects of [Ca 2+ ] i, PKC and PI 3K on the activation o f p38 were observed, but the activation of ERK and Akt were mainly regulated by PI 3 K Conclusion Thes e results suggest that both [Ca 2+ ] i dependent pathway(PKC ) and [Ca 2+ ] i independent pathway(PI 3 K, p38 and ERK)a re both important in the activation of NADPH oxidase

关 键 词：NADPH氧化酶 胞浆Ca^2+ FMLP HL-60细胞 白血病 信号转导 

分 类 号：R363[医药卫生—病理学]