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Eriodictyol Attenuates LPS-Induced Neuroinflammation, Amyloidogenesis, and Cognitive Impairments via the Inhibition of NF-κB in Male C57BL/6J Mice and BV2 Microglial Cells
Journal of Agricultural and Food Chemistry ( IF 5.7 ) Pub Date : 2018-09-13 00:00:00 , DOI: 10.1021/acs.jafc.8b03731
Pandi He 1 , Shikai Yan 1 , Jiaojiao Zheng 1 , Yuxing Gao 1 , Shuhan Zhang 1 , Zhigang Liu 1 , Xuebo Liu 1 , Chunxia Xiao 1
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Eriodictyol, a natural flavonoid mainly distributed in citrus fruits and peanut, has been well-documented with possession of excellent anti-inflammatory, antioxidant, and anticancer bioactivities. This work focus on the protective effects of eriodictyol on LPS-induced neuroinflammation, amyloidogenesis, cognitive impairment, and the potential mechanisms involved. Behavioral tests and histological examinations showed that eriodictyol significantly prevented the memory and neuronal damage triggered by LPS. Consistently, eriodictyol (100 mg/kg) reduced the formation of Aβ1–42 by 28.37 ± 16.71 pg/mL compared to the LPS group. In addition, high dose eriodictyol (100 mg/kg) also equilibrated the cholinergic system via suppressing AChE activity (0.1996 ± 0.0831 U/mgprot) and elevating ChAT activity (41.81 ± 24.72 U/g) as well as ACh level (5.093 ± 3.531 μg/mgprot) compared to the LPS group. Western blot results indicated that compared to the LPS group, eriodictyol suppressed LPS-induced glial overactivation (84.29% ± 27.21%) and regulated inflammatory mediators and cytokines by inhibiting the NF-κB and MAPK pathways. These results indicated that eriodictyol alleviated amyloidogenesis and memory impairment triggered by LPS via inhibiting TLR4, MAPKs, and PI3K/Akt, and activating Sirt1 pathways and thus blocking downstream translocation of NF-κB, which offers a potential nutritional preventive strategy for neuroinflammation diseases such as Alzheimer’s disease (AD).

中文翻译:

Eriodictyol通过抑制雄性C57BL / 6J小鼠和BV2小胶质细胞中的NF-κB减轻LPS诱导的神经炎症,淀粉样蛋白生成和认知障碍。

Eriodictyol是一种主要分布在柑橘类水果和花生中的天然类黄酮,据文献记载,它具有出色的抗炎,抗氧化和抗癌生物活性。这项工作的重点是Eriodictyol对LPS诱导的神经炎症,淀粉样蛋白生成,认知障碍和涉及的潜在机制的保护作用。行为学测试和组织学检查表明,雌三醇可明显预防LPS触发的记忆和神经元损伤。始终如一,雌黄酚(100 mg / kg)减少了Aβ1–42的形成与LPS组相比增加了28.37±16.71 pg / mL。此外,高剂量的雌黄醇(100 mg / kg)还可以通过抑制AChE活性(0.1996±0.0831 U / mgprot)和提高ChAT活性(41.81±24.72 U / g)以及ACh水平(5.093±3.531)来平衡胆碱能系统。与LPS组相比)。蛋白质印迹结果表明,与LPS组相比,芥酸间苯三酚可抑制LPS诱导的神经胶质过度活化(84.29%±27.21%),并通过抑制NF-κB和MAPK途径来调节炎症介质和细胞因子。这些结果表明,雌三醇通过抑制TLR4,MAPK和PI3K / Akt并激活Sirt1途径从而阻断NF-κB的下游移位,减轻了LPS触发的淀粉样蛋白生成和记忆障碍。
更新日期:2018-09-13
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