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首页> 外文期刊>Journal of neuroinflammation >Magnolia polyphenols attenuate oxidative and inflammatory responses in neurons and microglial cells
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Magnolia polyphenols attenuate oxidative and inflammatory responses in neurons and microglial cells

机译：玉兰多酚可减轻神经元和小胶质细胞的氧化和炎症反应

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Background The bark of magnolia has been used in Oriental medicine to treat a variety of remedies, including some neurological disorders. Magnolol (Mag) and honokiol (Hon) are isomers of polyphenolic compounds from the bark of Magnolia officinalis, and have been identified as major active components exhibiting anti-oxidative, anti-inflammatory, and neuroprotective effects. In this study, we investigate the ability of these isomers to suppress oxidative stress in neurons stimulated by the ionotropic glutamate receptor agonist N-methyl-D-aspartate (NMDA) and oxidative and inflammatory responses in microglial cells activated by interferon-γ (IFNγ) and lipopolysaccharide (LPS). We also attempt to elucidate the mechanism and signaling pathways involved in cytokine-induced production of reactive oxygen species (ROS) in microglial cells. Methods Dihydroethidium (DHE) was used to assay superoxide production in neurons, while CM-H2DCF-DA was used to test for ROS production in murine (BV-2) and rat (HAPI) immortalized microglial cells. NADPH oxidase inhibitors (for example, diphenyleneiodonium (DPI), AEBSF, and apocynin) and immunocytochemistry targeting p47phox and gp91phox were used to assess the involvement of NADPH oxidase. Western blotting was used to assess iNOS and ERK1/2 expression, and the Griess reaction protocol was employed to determine nitric oxide (NO) concentration. Results Exposure of Hon and Mag (1–10 μM) to neurons for 24 h did not alter neuronal viability, but both compounds (10 μM) inhibited NMDA-stimulated superoxide production, a pathway known to involve NADPH oxidase. In microglial cells, Hon and Mag inhibited IFNγ±LPS-induced iNOS expression, NO, and ROS production. Studies with inhibitors and immunocytochemical assay further demonstrated the important role of IFNγ activating the NADPH oxidase through the p-ERK-dependent pathway. Hon and, to a lesser extent, Mag inhibited IFNγ-induced p-ERK1/2 and its downstream pathway for ROS and NO production. Conclusion This study highlights the important role of NADPH oxidase in mediating oxidative stress in neurons and microglial cells and has unveiled the role of IFNγ in stimulating the MAPK/ERK1/2 signaling pathway for activation of NADPH oxidase in microglial cells. Hon and Mag offer anti-oxidative or anti-inflammatory effects, at least in part, through suppressing IFNγ-induced p-ERK1/2 and its downstream pathway.
机译：背景技术玉兰树皮已在东方医学中用于治疗多种疗法，包括某些神经系统疾病。厚朴酚（Mag）和厚朴酚（Hon）是木兰皮中多酚化合物的异构体，已被确定为主要的抗氧化，抗炎和神经保护活性成分。在这项研究中，我们研究了这些异构体抑制离子型谷氨酸受体激动剂N-甲基-D-天冬氨酸（NMDA）刺激的神经元中氧化应激的能力以及干扰素-γ（IFNγ）激活的小胶质细胞的氧化和炎症反应。和脂多糖（LPS）。我们还试图阐明在小胶质细胞中细胞因子诱导的活性氧物质（ROS）产生的机制和信号通路。方法用二氢乙啶（DHE）测定神经元中超氧化物的产生，而用CM-H2DCF-DA检验永生的小胶质细胞（BV-2）和大鼠（HAPI）中的ROS产生。 NADPH氧化酶抑制剂（例如，二亚苯基碘鎓（DPI），AEBSF和载脂蛋白）和针对p47phox和gp91phox的免疫细胞化学用于评估NADPH氧化酶的参与。使用蛋白质印迹法评估iNOS和ERK1 / 2的表达，并使用Griess反应方案确定一氧化氮（NO）的浓度。结果Hon和Mag（1–10μM）暴露于神经元24 h不会改变神经元的生存能力，但是两种化合物（10μM）均抑制NMDA刺激的超氧化物生成，这是一种涉及NADPH氧化酶的途径。在小胶质细胞中，Hon和Mag抑制IFNγ±LPS诱导的iNOS表达，NO和ROS产生。抑制剂和免疫细胞化学测定的研究进一步证明了IFNγ通过p-ERK依赖性途径激活NADPH氧化酶的重要作用。 Hon和Mag在较小程度上抑制了IFNγ诱导的p-ERK1 / 2及其下游产生ROS和NO的途径。结论这项研究突出了NADPH氧化酶在介导神经元和小胶质细胞氧化应激中的重要作用，并揭示了IFNγ刺激MAPK / ERK1 / 2信号通路激活小胶质细胞中NADPH氧化酶的作用。 Hon和Mag至少部分地通过抑制IFNγ诱导的p-ERK1 / 2及其下游途径来提供抗氧化或抗炎作用。

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