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韩国红参通过下调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模型中的脊髓脱髓鞘。

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.

作者信息

Lee Min Jung, Chang Byung Joon, Oh Seikwan, Nah Seung-Yeol, Cho Ik-Hyun

机构信息

Department of Convergence Medical Science, College of Korean Medicine, Kyung Hee University, Seoul, Republic of Korea.

Department of Anatomy, College of Veterinary Medicine, Konkuk University, Seoul, Republic of Korea.

出版信息

J Ginseng Res. 2018 Oct;42(4):436-446. doi: 10.1016/j.jgr.2017.04.013. Epub 2017 May 8.

Abstract

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) 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 kinase/nuclear 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.

摘要

背景

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尚未得到充分研究。

方法

我们使用了一种多发性硬化症的急性实验性自身免疫性脑脊髓炎动物模型,确定了KRGE对脊髓髓鞘形成的影响和机制。

结果

在用髓鞘碱性蛋白(MBP)肽免疫前10天,口服KRGE(100mg/kg)预处理对脊髓脱髓鞘具有保护作用,可抑制包括小胶质细胞在内的免疫细胞的募集和激活,降低有害炎症介质(白细胞介素-6、干扰素-γ和环氧化酶-2)的mRNA表达,但增加保护性炎症介质(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)的mRNA表达。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信号通路的显著下调有关。

结论

我们的研究结果表明,KRGE通过抑制p38丝裂原活化蛋白激酶/核因子-κB信号通路的激活来减轻急性实验性自身免疫性脑脊髓炎中的脊髓脱髓鞘。因此,KRGE可能用作治疗多发性硬化症等自身免疫性疾病的新疗法,尽管还需要进一步研究。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9612/6187097/acca34ad0344/gr1.jpg

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