首页> 外文期刊>Neurochemical research >kappa-Carrageenan Oligosaccharides Inhibit the Inflammation of Lipopolysaccharide-Activated Microglia Via TLR4/NF-kappa B and p38/JNK MAPKs Pathways
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kappa-Carrageenan Oligosaccharides Inhibit the Inflammation of Lipopolysaccharide-Activated Microglia Via TLR4/NF-kappa B and p38/JNK MAPKs Pathways

机译:κ-卡拉胶低聚糖通过TLR4/NF-κB 和 p38/JNK MAPKs 通路抑制脂多糖活化小胶质细胞的炎症

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摘要

Microglial inflammation plays an essential role in neurodegenerative disease. Our previous studies had shown that kappa-carrageenan oligosaccharides (KOS) could inhibit the excessive activation of microglia that induced by LPS, while the interrelated mechanisms were still indistinct. Therefore, we detected the inflammatory signaling pathway on LPS-activated microglia that pretreat by different content of KOS to reveal the mechanism on KOS's inhibition of microglia inflammatory response. ELISA was used to detect the effects of KOS on the secretion of interleukin-1 (IL-1 beta), tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6) and prostaglandin E2 (PG-2) by LPS-activated microglia, respectively. The production of reactive oxygen species (ROS) and nitric oxide (NO) in microglia cells was detected by flow cytometry, and the protein expression of immunoinflammation-related signaling pathways were detected by Western Blot. The results showed that KOS could significantly protected the microglia from the over-activated inflammatory by inhibiting the release of inflammatory cytokines and the oxidative stress response. And KOS could reduce the expression of the protein that related to the TLR4/NF-kappa B and p38/JNK MAPKs pathways activated by LPS in microglia. However, there may be no specific target of KOS in cells. Therefore, KOS, a natural algal source oligosaccharide, has immunomodulatory effects and can be used as a potential intervention therapy for inflammatory related neurodegenerative diseases.
机译:小胶质细胞炎症在神经退行性疾病中起着至关重要的作用。我们之前的研究表明,κ-卡拉胶低聚糖(KOS)可以抑制LPS诱导的小胶质细胞的过度活化,但相互关联的机制仍然不明确。因此,我们检测了不同KOS含量预处理的LPS激活小胶质细胞的炎症信号通路,揭示了KOS抑制小胶质细胞炎症反应的机制。ELISA检测KOS对LPS激活小胶质细胞分泌白细胞介素-1(IL-1 beta)、肿瘤坏死因子-α(TNF-α)、白细胞介素-6(IL-6)和前列腺素E2(PG-2)的影响。流式细胞术检测小胶质细胞中活性氧(ROS)和一氧化氮(NO)的产生,Western Blot检测免疫炎症相关信号通路的蛋白表达。结果表明,KOS可以通过抑制炎性细胞因子的释放和氧化应激反应来显著保护小胶质细胞免受过度激活的炎症。KOS可以降低小胶质细胞中LPS激活的TLR4/NF-kappa B和p38/JNK MAPKs通路相关蛋白的表达。然而,细胞中可能没有KOS的特异性靶点。因此,KOS是一种天然藻源低聚糖,具有免疫调节作用,可作为炎症相关神经退行性疾病的潜在干预疗法。

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