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首页> 外文期刊>Journal of Ginseng Research >Korean Red Ginseng mitigates spinal demyelination in a model of acute multiple sclerosis by downregulating p38 mitogen-activated protein kinase and nuclear factor-κB signaling pathways
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Korean Red Ginseng mitigates spinal demyelination in a model of acute multiple sclerosis by downregulating p38 mitogen-activated protein kinase and nuclear factor-κB signaling pathways

机译:高丽红参可通过下调p38丝裂原活化蛋白激酶和核因子-κB信号通路减轻急性多发性硬化症模型中的脊髓脱髓鞘

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Background The potential therapeutic values of Korean Red Ginseng extract (KRGE) in autoimmune disorders of nervous system have not been fully investigated. Methods We used an acute experimental autoimmune encephalomyelitis animal model of multiple sclerosis and determined the effects and mechanism of KRGE on spinal myelination. Results Pretreatment with KRGE (100 mg/kg, orally) for 10 days before immunization with myelin basic protein (MBP)68–82 peptide exerted a protective effect against demyelination in the spinal cord, with inhibited recruitment and activation of immune cells including microglia, decreased mRNA expression of detrimental inflammatory mediators (interleukin-6, interferon-γ, and cyclooxygenase-2), but increased mRNA expression of protective inflammatory mediators (insulin-like growth factor β1, transforming growth factor β, and vascular endothelial growth factor-1). These results were associated with significant downregulation of p38 mitogen-activated protein kinase and nuclear factor-κB signaling pathways in microglia/macrophages, T cells, and astrocytes. Conclusion Our findings suggest that KRGE alleviates spinal demyelination in acute experimental autoimmune encephalomyelitis through inhibiting the activation of the p38 mitogen-activated protein kinaseuclear factor-κB signaling pathway. Therefore, KRGE might be used as a new therapeutic for autoimmune disorders such as multiple sclerosis, although further investigation is needed.
机译:背景技术尚未完全研究韩国红参提取物(KRGE)在神经系统自身免疫性疾病中的潜在治疗价值。方法采用急性多发性硬化的自身免疫性脑脊髓炎动物实验模型,确定KRGE对脊髓髓鞘形成的作用和机制。结果在用髓磷脂碱性蛋白(MBP) 68-82 肽免疫之前,用KRGE(100 mg / kg口服)预处理10天对脊髓脱髓鞘具有保护作用,抑制了募集和抑制。激活包括小胶质细胞在内的免疫细胞,降低有害炎症介质(白介素-6,干扰素-γ和环氧合酶-2)的mRNA表达,但保护性炎症介质(胰岛素样生长因子β1,转化生长因子β,和血管内皮生长因子-1)。这些结果与小胶质细胞/巨噬细胞,T细胞和星形胶质细胞中p38丝裂原活化蛋白激酶和核因子-κB信号通路的显着下调有关。结论我们的发现表明,KRGE通过抑制p38丝裂原激活的蛋白激酶/核因子-κB信号通路的激活,减轻了急性实验性自身免疫性脑脊髓炎的脊髓脱髓鞘。因此,尽管需要进一步研究,KRGE可能被用作自身免疫性疾病(如多发性硬化症)的新疗法。

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