The inhibitory action of butyrate on lipopolysaccharide-induced nitric oxide production in RAW 264.7 murine macrophage cells
The inhibitory action of butyrate on lipopolysaccharide-induced nitric oxide production in RAW 264.7 murine macrophage cells
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DOI：
10.1179/096805100101532108
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发表时间：
2000-01-01
期刊：
影响因子：
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通讯作者：
Yokochi, T
中科院分区：
文献类型：
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作者：
Chakravortty, D;Koide, N;Yokochi, T
研究了结肠菌群的天然细菌产物丁酸盐对内毒素诱导的RAW 264.7小鼠巨噬细胞产生一氧化氮的影响。丁酸盐可显著减少内毒素刺激的原始细胞中NO的产生。这种抑制作用被丁酸盐的去除所消除。丁酸盐还能抑制脂多糖刺激的RAW细胞诱导型一氧化氮合酶(INOS)的表达。此外，丁酸盐通过稳定I-kappa B-α和I-kappa B-β来抑制核因子-kappaB的激活。丁酸盐不影响脂多糖对丝裂原活化蛋白(MAP)激酶的磷酸化。因此，我们认为丁酸通过抑制iNOS的表达而下调内毒素诱导的原始细胞NO的产生，这可能是由于丁酸抑制了核因子-kappaB的活化。
The effect of butyrate, a natural bacterial product of colonic bacterial flora, on lipopolysaccharide (LPS)-induced nitric oxide (NO) production in RAW 264.7 murine macrophage cells was studied. Butyrate significantly reduced NO production in LPS-stimulated RAW cells. The inhibition was abolished by the removal of butyrate. Butyrate also inhibited the expression of inducible type NO synthase (iNOS) in LPS-stimulated RAW cells. Furthermore, butyrate prevented the activation of nuclear factor (NF)-kappa B through the stabilization of I kappa B-alpha and I kappa B-beta. Butyrate did not affect the phosphorylation of mitogen-activated protein (MAP) kinases by LPS. It was, therefore, suggested that butyrate down-regulated LPS-induced NO production in RAW cells through preventing the expression of iNOS, and that it was due to the inhibitory action of butyrate on the activation of NF-kappa B.