Stimulation and inhibition of nitric oxide production in macrophages and neural cells as observed by spin trapping.

Stimulation and inhibition of nitric oxide production in macrophages and neural cells as observed by spin trapping.
复制标题

通过自旋捕获观察到巨噬细胞和神经细胞中一氧化氮产生的刺激和抑制。

DOI:
10.1016/s0891-5849(96)00217-1
复制
发表时间:
1997
影响因子:
7.4
通讯作者:
Clarkson,RB
Clarkson,RB
中科院分区:
医学1区
文献类型:
--
作者:
Norby,SW;Weyhenmeyer,JA;Clarkson,RB

文献摘要

被引文献

相似文献

我们结合了电子顺磁共振(EPR)和自旋捕获技术来测量体外激活的巨噬细胞和神经细胞产生的一氧化氮(NO)。细菌脂多糖 (LPS)、γ 干扰素 (IFNγ) 或两者刺激的巨噬细胞产生 NO。 KCl 和 CaCl2、N-甲基-d-天冬氨酸 (NMDA) 和 IFNγ 激活的分化和未分化神经细胞也能产生 NO。神经细胞的激活机制可能是通过通道或受体。当连续或同时施用 LPS 和 IFNγ 组合刺激时,巨噬细胞中的 NO 产量达到最大。 IFNγ是对神经细胞最有效的刺激剂。所有这些细胞体外产生的 NO 均被 NG-单甲基 L-精氨酸 (l-NMMA) 以剂量依赖性方式抑制。当细胞在不含 L-精氨酸的培养基中生长时,NO 产生被完全抑制,表明 L-精氨酸对于 NO 产生至关重要。我们还从我们的研究中得出结论,与神经细胞中观察到的相比,巨噬细胞中 NO 的产生量更大且持续时间更长。版权所有 © 1996 Elsevier Science Inc.
We have combined electron paramagnetic resonance (EPR) and spin trapping techniques to measure nitric oxide (NO) production by activated macrophages and neural cells in vitro. Macrophages stimulated by bacterial lipopolysaccharide (LPS), gamma interferon (IFNγ), or both, produced NO. Differentiated and undifferentiated neural cells activated by KCl and CaCl2, N-methyl-d-aspartate (NMDA), and IFNγ were shown to produce NO as well. The mechanism of activation in neural cells could be either by channels or receptors. Maximum NO production in macrophages was achieved when stimulated by a combination of LPS and IFNγ administered sequentially or concurrently. IFNγ was the most effective stimulant for neural cells. The in vitro production of NO by all these cells was inhibited by NG-monomethyl l-arginine (l-NMMA) in a dose-dependent manner. Complete inhibition of NO production occurred when cells were grown in l-arginine free medium, indicating that l-arginine was essential for NO production. We also concluded from our study that NO production in macrophages was in greater amounts and more long lasting in duration than that observed in the neural cells.Copyright © 1996 Elsevier Science Inc.