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首页> 外文期刊>Neurochemical research >HMGB1-TLR4 Axis Plays a Regulatory Role in the Pathogenesis of Mesial Temporal Lobe Epilepsy in Immature Rat Model and Children via the p38MAPK Signaling Pathway
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HMGB1-TLR4 Axis Plays a Regulatory Role in the Pathogenesis of Mesial Temporal Lobe Epilepsy in Immature Rat Model and Children via the p38MAPK Signaling Pathway

机译：HMGB1-TLR4轴在未成熟的大鼠模型和儿童通过P38MAPK信号通路中发病机制中发病作用

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摘要

The HMGB1-TLR4 axis is activated in adult mouse models of acute and chronic seizure. Nevertheless, whether HMGB1 was involved in the pathogenesis of mesial temporal lobe epilepsy ( MTLE) remains unknown. In this study, we first measured the dynamic expression patterns of HMGB1 and TLR4 in the hippocampi of a rat model and in children with MTLE, as well as the levels of TNF-alpha and IL-1 beta. In addition, HMGB1 was added to mimic the process of inflammatory response in neurons. Neuronal somatic size and dendritic length were measured by immunohistochemistry and digital imaging. The results showed that the expression of HMGB1 and TLR4 as well as the levels of TNF-alpha and IL-1 beta were higher in the three stages of MTLE development in the rat model and in the children with MTLE. HMGB1 increased the levels of TNF-alpha and IL-1 beta, upregulated the protein level of p-p38MAPK and promoted the growth of cell somatic size and dendritic length in neurons. Pre-treatment with p38MAPK inhibitor SB203580 decreased the levels of TNF-alpha and IL-1 beta, while downregulation of TLR4 significantly reduced HMGB1induced p38MAPK signaling pathway activation. These data demonstrated that the HMGB1-TLR4 axis may play an important role in the pathogenesis of MTLE via the p38MAPK signaling pathway.
机译：HMGB1-TLR4轴在急性和慢性癫痫发作的成人小鼠模型中激活。然而，HMGB1是否参与了薄膜颞叶癫痫（咒语）的发病机制仍然未知。在这项研究中，我们首先测量大鼠模型的海马和粪便儿童的HMGB1和TLR4的动态表达模式，以及TNF-α和IL-1β的水平。此外，加入HMGB1以模仿神经元炎症反应的过程。通过免疫组织化学和数字成像测量神经元体细胞大小和树突长度。结果表明，HMGB1和TLR4的表达以及TNF-α和IL-1β的水平在大鼠模型和粪便中的儿童的三个阶段在案牙中的三个阶段较高。 HMGB1增加了TNF-α和IL-1β的水平，上调了P-P38MAPK的蛋白质水平，并促进了神经元细胞体细胞大小和树枝状长度的生长。用P38MAPK抑制剂SB203580预处理降低了TNF-α和IL-1β的水平，而TLR4的下调显着降低了HMGB1诱导的P38MAPK信号通路活化。这些数据证明HMGB1-TLR4轴可能在咒语的发病机制中通过P38MAPK信号通路发挥重要作用。

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  • 来源
    《Neurochemical research》 |2017年第4期|共12页
  • 作者

    Yang Weihong; Li Jing; Shang Yun; Zhao Li; Wang Mingying; Shi Jipeng; Li Shujun;

  • 作者单位

    Xinxiang Med Coll Dept Nursing Affiliated Hosp 1 Xinxiang 453100 Peoples R China;

    Xinxiang Med Coll Dept Pediat Affiliated Hosp 1 Xinxiang 453100 Peoples R China;

    Xinxiang Med Coll Dept Neonatol Affiliated Hosp 1 Xinxiang 453100 Peoples R China;

    Xinxiang Med Coll PICU Affiliated Hosp 1 88 Jian Kang Rd Xinxiang 453100 Peoples R China;

    Xinxiang Med Coll PICU Affiliated Hosp 1 88 Jian Kang Rd Xinxiang 453100 Peoples R China;

    Xinxiang Med Coll Dept Neonatol Affiliated Hosp 1 Xinxiang 453100 Peoples R China;

    Xinxiang Med Coll PICU Affiliated Hosp 1 88 Jian Kang Rd Xinxiang 453100 Peoples R China;

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  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 生物体其他化学成分;
  • 关键词

    HMGB1; P38MAPK; TLR4; Mesial temporal lobe epilepsy;

    机译：HMGB1;P38MAPK;TLR4;弱小的颞叶癫痫;

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