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首页> 外文期刊>Journal of pharmacological sciences. >Nitric oxide inhibits lipopolysaccharide-induced inducible nitric oxide synthase expression and its own production through the cGMP signaling pathway in murine microglia BV-2 cells
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Nitric oxide inhibits lipopolysaccharide-induced inducible nitric oxide synthase expression and its own production through the cGMP signaling pathway in murine microglia BV-2 cells

机译：一氧化氮通过cGMP信号通路抑制鼠小胶质细胞BV-2细胞中脂多糖诱导的一氧化氮合酶的表达及其自身产生

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摘要

The present study examined the effect of the nitric oxide (NO) donor NOC18 on lipopolysaccharide (LPS)-induced NO production to investigate a regulation mechanism of NO production by microglial cells. LPS increased the levels of NO and inducible NO synthase (iNOS) protein in BV-2 murine microglial cells in a concentration-dependent manner. Pretreatment with NOC18 for 24 h concentration-dependently attenuated the LPS-induced iNOS protein expression and NO production. The inhibitory effect of NOC18 on LPS-induced NO production was partially blocked by LY83583, a soluble guanylate cyclase inhibitor. Pretreatment with dibutyryl guanosine-3′,5′-cyclic monophosphate (DBcGMP), a cell-permeable cGMP analogue, for 24 h attenuated partially LPS-induced iNOS protein expression and NO production. Furthermore, the effects of LPS on iNOS and NO production were inhibited by the c-Jun N-terminal kinase (JNK) inhibitor SP600125, and LPS-induced phosphorylation of JNK and c-Jun was inhibited by NOC18 and DBcGMP. These results suggest that NO production by microglial cells is controlled by a negative feedback mechanism via the NO/cGMP signaling pathway.
机译：本研究检查了一氧化氮（NO）供体NOC18对脂多糖（LPS）诱导的NO产生的影响，以研究小胶质细胞产生NO的调节机制。 LPS以浓度依赖的方式增加BV-2鼠小胶质细胞中NO和诱导型NO合酶（iNOS）蛋白的水平。用NOC18预处理24小时浓度依赖性减弱LPS诱导的iNOS蛋白表达和NO产生。可溶性鸟苷酸环化酶抑制剂LY83583部分阻止了NOC18对LPS诱导的NO产生的抑制作用。用二丁酰鸟苷-3'，5'-环状单磷酸酯（DBcGMP）（一种细胞可渗透的cGMP类似物）预处理24小时，可部分减弱LPS诱导的iNOS蛋白表达和NO产生。此外，c-Jun N末端激酶（JNK）抑制剂SP600125抑制LPS对iNOS和NO产生的影响，而NOC18和DBcGMP抑制LPS诱导的JNK和c-Jun磷酸化。这些结果表明，小胶质细胞的NO产生是通过NO / cGMP信号传导途径的负反馈机制来控制的。

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