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首页> 外文期刊>Brain research >MS275 reduces seizure-induced brain damage in developing rats by regulating p38 MAPK signaling pathways and epigenetic modification
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MS275 reduces seizure-induced brain damage in developing rats by regulating p38 MAPK signaling pathways and epigenetic modification

机译：MS275通过调节P38 MAPK信号通路和表观遗传改性，减少癫痫发育诱导的脑损伤

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摘要

Seizure is a common acute and severe disease in infants and children. Recurrent seizures or persistent seizures may cause irreversible brain damage. Mitogen activated protein kinase (MAPK) signaling pathway is associated with an inflammatory response, however it's involvement in the pathological process of seizures is not clear. Histone deacetylase inhibitors (HDACi) have promising neuroprotective effects through epigenetic regulation. Therefore, this study aimed to investigate the mechanism of HDACi MS275 on p38 MAPK signaling pathway and p38 histone modifications in developing rats post-seizure. Intraperitoneal administration of Pentylenetetrazole (PTZ) was used to induce developing rat seizures, and MS275 (5 or 10 mg/kg) was injected intraperitoneally 2 h before PTZ injection. Hippocampal tissues were sampled at 24 h post-seizures for protein and mRNA levels of p38, MK2, CREB and IL-6. Neuronal apoptosis and microglia activation significantly increased after PTZ treatment. However, pretreatment with MS275 attenuated these effects as well as increased seizure latency and decreased seizure scores. Furthermore, MS275 was found to inhibit the expression of p38 by increasing histone H3 and H4 acetylation and decreasing histone H3 and H4 methylation. This study thereby demonstrates that HDACi MS275 can reduce the inflammatory response associated with seizure-induced brain injury through inhibiting the p38 MAPK signaling pathway and p38 gene expression.
机译：癫痫发作是婴儿和儿童的常见急性和严重疾病。复发性癫痫发作或持续癫痫发作可能导致不可逆的脑损伤。丝裂原激活蛋白激酶（MAPK）信号传导途径与炎症反应有关，但它参与癫痫发作的病理过程尚不清楚。组蛋白脱乙酰酶抑制剂（HDACI）通过表观遗传调控有希望的神经保护作用。因此，本研究旨在研究HDACI MS275对癫痫发作大鼠的P38 MAPK信号通路和P38组蛋白修饰的方法。使用腹膜内四唑（PTZ）诱导显影大鼠癫痫发作，并在PTZ注射之前腹膜内注射MS 275（5或10mg / kg）。在24小时的蛋白质和mRNA水平的24小时内取样海马组织，P38，MK2，CREB和IL-6的蛋白质和mRNA水平。 PTZ治疗后神经元细胞凋亡和小胶质细胞活化显着增加。然而，使用MS275的预处理减弱了这些效果以及增加的癫痫发作等待时间和减少癫痫发作评分。此外，发现MS275通过增加组蛋白H3和H4乙酰化和降低组蛋白H3和H4甲基化来抑制P38的表达。因此，该研究表明HDACI MS275可以通过抑制P38 MAPK信号通路和P38基因表达，降低与癫痫发作诱导的脑损伤相关的炎症反应。

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  • 来源
    《Brain research》 |2020年第1期|共9页
  • 作者

    Hu Qing-peng; Huang Xiang-yi; Peng Fang; Yang Hui; Wu Can;

  • 作者单位

    Univ South China Hosp 2 Dept Pediat Hengyang 421001 Hunan Peoples R China;

    Univ South China Hosp 2 Dept Funct Examinat 35 Jiefang Rd Hengyang 421001 Hunan Peoples R;

    Univ South China Hosp 2 Dept Pediat Hengyang 421001 Hunan Peoples R China;

    Univ South China Hosp 2 Dept Pediat Hengyang 421001 Hunan Peoples R China;

    Univ South China Hosp 2 Dept Pediat Hengyang 421001 Hunan Peoples R China;

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  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 神经病学;
  • 关键词

    MS275; Seizures; P38; Histone; Epigenetic modification;

    机译：MS275;癫痫发作;P38;组蛋白;表观遗传修饰;

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