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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 NADPH氧化酶激活都起着重要作用
Objective To clarify the role of [Ca2 +] i and some kinases in the activation of NADPH oxidase in neutrophils and the signal transduction pathway of NADPH oxidase activation. Methods The effect of [Ca2 +] i and certain kinases on the activation of NADPH oxidase by f ML P was studied using neutrophil-like HL-60 cells. Results After the [Ca2 +] i was removed with 10μmol / L BAPTA-AM, the production of O-2 was significantly reduced. The PKC inhibitor 92103 at 8μmol / L significantly inhibited the production of O-2. L of p3 8 inhibitor SB2 0 3 5 80,5 0 μmol / L of the ERK inhibitor PD0 980 5 9 and 0. 1μm ol / L PI3K inhibitor Wortm annin O 2 production was inhibited to varying degrees; PKC , PI3K, p38 and ERK activation had no effect on the increase of [Ca2 +] i; [Ca2 +] i, PKC and PI3K had some effect on p38 activation, while ERK and Akt activation were mainly regulated by PI3-K. CONCLUSIONS [Ca2 +] i dependent pathway (PKC) and [Ca2 +] i independent pathways (PI3K, p38 and ERK) play an important role in NADPH oxidase activation