首页> 美国卫生研究院文献>PLoS Clinical Trials >Neuroprotective Effect of Kaempferol Glycosides against Brain Injury and Neuroinflammation by Inhibiting the Activation of NF-κB and STAT3 in Transient Focal Stroke
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Neuroprotective Effect of Kaempferol Glycosides against Brain Injury and Neuroinflammation by Inhibiting the Activation of NF-κB and STAT3 in Transient Focal Stroke

机译:山emp酚糖苷通过抑制短暂性局灶性中风中NF-κB和STAT3的活化对脑损伤和神经炎症的神经保护作用。

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摘要

BackgroundIschemic brain injury is associated with neuroinflammatory response, which essentially involves glial activation and neutrophil infiltration. Transcription factors nuclear factor-κB (NF-κB) and signal transducer and activator of transcription 3 (STAT3) contribute to ischemic neuroinflammatory processes and secondary brain injury by releasing proinflammatory mediators. Kaempferol-3-O-rutinoside (KRS) and kaempferol-3-O- glucoside (KGS) are primary flavonoids found in Carthamus tinctorius L. Recent studies demonstrated that KRS protected against ischemic brain injury. However, little is known about the underlying mechanisms. Flavonoids have been reported to have antiinflammatory properties. Herein, we explored the effects of KRS and KGS in a transient focal stroke model.
机译:背景缺血性脑损伤与神经炎症反应相关,其本质上涉及神经胶质激活和中性粒细胞浸润。转录因子核因子-κB(NF-κB)和信号转导和转录激活因子3(STAT3)通过释放促炎性介质而促进缺血性神经炎症过程和继发性脑损伤。山茱fer醇-3-O-芸香糖苷(KRS)和山茱fer醇-3-O-葡糖苷(KGS)是红花中发现的主要类黄酮。最近的研究表明,KRS可以防止缺血性脑损伤。但是,对于底层机制知之甚少。据报道类黄酮具有抗炎特性。在本文中,我们探讨了KRS和KGS在短暂性中风模型中的作用。

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