Differential effects of pentoxifylline and interleukin-10 on production of tumor necrosis factor and inducible nitric oxide synthase by murine macrophages.
Differential effects of pentoxifylline and interleukin-10 on production of tumor necrosis factor and inducible nitric oxide synthase by murine macrophages.
复制标题
己酮可可碱和白细胞介素 10 对小鼠巨噬细胞产生肿瘤坏死因子和诱导型一氧化氮合酶的不同影响。
DOI：
10.1086/513960
复制
发表时间：
1997
期刊：
影响因子：
--
通讯作者：
English,BK
中科院分区：
文献类型：
--
作者：
Loftis,LL;Meals,EA;English,BK
本文比较了戊茶碱和重组白细胞介素-10（rIL-10）对小鼠巨噬细胞产生肿瘤坏死因子（TNF）和诱导型一氧化氮合酶（iNOS）的抑制作用。无论刺激物是细菌脂多糖（LPS）、重组干扰素-γ（rIFN-γ）还是LPS + rIFN-γ，喷替福林均以剂量依赖性方式持续抑制TNF和iNOS的蓄积。类似地，rIL-10一致性地减少用LPS、rIFN-γ或LPS加rIFN-γ刺激的细胞的TNF产生。然而，rIL-10微弱地抑制LPS诱导的iNOS产生，但未能阻断（并且常常增强）rIFN-γ诱导的iNOS产生。喷替福林和rIL-10的组合导致TNF的相加或协同抑制，但不是iNOS的产生;事实上，rIL-10似乎干扰喷替福林阻断iNOS积累的能力。这些数据表明，抗炎药的组合可能对炎症介质的产生产生产生意想不到的影响。
The abilities of pentoxifylline and recombinant interleukin-10 (rIL-10) to inhibit tumor necrosis factor (TNF) and inducible nitric oxide synthase (iNOS) production in RAW264.7 murine macrophages were compared. Pentoxifylline consistently inhibited the accumulation of both TNF and iNOS in a dose-dependent manner whether the stimulus was bacterial lipopolysaccharide (LPS), recombinant interferon-γ (rIFN-γ), or LPS plus rIFN-γ. Similarly, rIL-10 consistently reduced TNF production by cells stimulated with LPS, rIFN-γ, or LPS plus rIFN-γ. However, rIL-10 weakly inhibited LPS-induced iNOS production but failed to block (and often augmented) rIFN-γ-induced iNOS production. Combinations of pentoxifylline and rIL-10 led to additive or synergistic inhibition of TNF but not iNOS production; in fact, rIL-10 appeared to interfere with the ability of pentoxifylline to block iNOS accumulation. These data suggest that combinations of antiinflammatory agents may have unanticipated effects on inflammatory mediator production.