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首页> 外文期刊>Journal of endotoxin research >Butyrate enhances the production of nitric oxide in mouse vascular endothelial cells in response to gamma interferon.
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Butyrate enhances the production of nitric oxide in mouse vascular endothelial cells in response to gamma interferon.

机译:丁酸可增强小鼠血管内皮细胞对伽马干扰素产生的一氧化氮的产生。

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摘要

The effect of butyrate, a natural bacterial product of colonic bacterial flora, on nitric oxide (NO) production in murine vascular endothelial cell line END-D in response to IFN-gamma and/or LPS was studied. Butyrate significantly augmented NO production in END-D cells in response to IFN-gamma or IFN-gamma + LPS, but not LPS alone. The NO production was augmented by the addition of butyrate until 6 h after the stimulation with IFN-gamma or IFN-gamma + LPS. The augmentation was abolished by the removal of butyrate from the cultures. Butyrate enhanced the expression of inducible type NO synthase (iNOS) in the stimulated END-D cells. Furthermore, butyrate-enhanced NO production in the presence of various signal inhibitors down-regulating the signal pathways using nuclear factor (NF)-kappaB, mitogen-activated protein (MAP) kinases and Janus tyrosine kinase. The putative mechanism of butyrate-induced augmentation of NO production in response to IFN-gamma or IFN-gamma + LPS is discussed.
机译:研究了丁酸,一种结肠细菌菌群的天然细菌产物,对鼠血管内皮细胞系END-D中的一氧化氮(NO)产生的影响,该细胞响应IFN-γ和/或LPS。丁酸酯显着增加了END-D细胞对IFN-γ或IFN-γ+ LPS的反应,但没有单独产生LPS。通过添加丁酸盐直到用IFN-γ或IFN-γ+ LPS刺激后6小时增加NO的产生。通过从培养物中除去丁酸盐来取消增加。丁酸盐可增强刺激的END-D细胞中诱导型NO合酶(iNOS)的表达。此外,在存在各种信号抑制剂的情况下,使用核因子(NF)-κB,有丝分裂原激活的蛋白(MAP)激酶和Janus酪氨酸激酶可降低丁酸的NO生成,从而下调信号通路。讨论了丁酸诱导的NO产生对IFN-γ或IFN-γ+ LPS响应的增加的推测机制。

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