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首页> 外文期刊>The Journal of Nutritional Biochemistry >Luteolin inhibits cytokine expression in endotoxin/cytokine-stimulated microglia.
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Luteolin inhibits cytokine expression in endotoxin/cytokine-stimulated microglia.

机译：木犀草素抑制内毒素/细胞因子刺激的小胶质细胞中细胞因子的表达。

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摘要

Microglial activation plays a pivotal role in the pathogenesis of neurodegenerative disease by producing excessive proinflammatory cytokines and nitric oxide (NO). Luteolin, a naturally occurring polyphenolic flavonoid antioxidant, has potent anti-inflammatory and neuroprotective properties both in vitro and in vivo. However, the molecular mechanism of luteolin-mediated immune modulation in microglia is not fully understood. In the present study, we report the inhibitory effect of luteolin on lipopolysaccharide (LPS)/interferon gamma (IFN- gamma)-induced NO and proinflammatory cytokine production in rat primary microglia and BV-2 microglial cells. Luteolin concentration-dependently abolished LPS/IFN- gamma-induced NO, tumor necrosis factor alpha (TNF- alpha) and interleukin 1 beta (IL-1 beta) production as well as inducible nitric oxide synthase (iNOS) protein and mRNA expression. Luteolin exerted an inhibitory effect on transcription factor activity including nuclear factor kappaB (NF- kappaB), signal transducer and activator of transcription 1 (STAT1) and interferon regulatory factor 1 (IRF-1) in LPS/IFN- gamma-activated BV-2 microglial cells. Biochemical and pharmacological studies revealed that the anti-inflammatory effect of luteolin was accompanied by down-regulation of extracellular signal-regulated kinase (ERK), p38, c-Jun N-terminal kinase (JNK), Akt and Src. Further studies have demonstrated that the inhibitory effect of luteolin on intracellular signaling execution and proinflammatory cytokine expression is associated with resolution of oxidative stress and promotion of protein phosphatase activity. Together, these results suggest that luteolin suppresses NF- kappaB, STAT1 and IRF-1 signaling, thus attenuating inflammatory response of brain microglial cells. All rights reserved, Elsevier.
机译：小胶质细胞活化通过产生过量的促炎细胞因子和一氧化氮（NO）在神经退行性疾病的发病机理中起关键作用。木犀草素，一种天然存在的多酚类黄酮抗氧化剂，在体外和体内均具有有效的抗炎和神经保护特性。但是，尚未充分了解小胶质中木犀草素介导的免疫调节的分子机制。在本研究中，我们报道了木犀草素对大鼠原发性小胶质细胞和BV-2小胶质细胞中脂多糖（LPS）/干扰素γ（IFN-γ）诱导的NO和促炎性细胞因子产生的抑制作用。木犀草素浓度依赖性地消除了LPS /IFN-γ诱导的NO，肿瘤坏死因子α（TNF-α）和白介素1 beta（IL-1 beta）的产生以及诱导型一氧化氮合酶（iNOS）蛋白和mRNA的表达。木犀草素对LPS /IFN-γ激活的BV-2中的核因子kappaB（NF- kappaB），信号转导和转录激活因子1（STAT1）和干扰素调节因子1（IRF-1）发挥抑制作用。小胶质细胞。生化和药理研究表明，木犀草素的抗炎作用伴随着细胞外信号调节激酶（ERK），p38，c-Jun N端激酶（JNK），Akt和Src的下调。进一步的研究表明，木犀草素对细胞内信号传导执行和促炎性细胞因子表达的抑制作用与氧化应激的消除和蛋白磷酸酶活性的提高有关。在一起，这些结果表明木犀草素抑制NF-κB，STAT1和IRF-1信号传导，从而减弱脑小胶质细胞的炎症反应。保留所有权利，Elsevier。

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