关键词: CCL2 HMGB1 IL-33 TLR-4 TNF-a biomarkers drug resistant epilepsy epileptogenesis neuroinflammation sTNFr2

Mesh : Humans Biomarkers Neuroinflammatory Diseases / diagnosis metabolism HMGB1 Protein / metabolism Epilepsy / diagnosis metabolism Cytokines / metabolism Toll-Like Receptor 4 / metabolism Drug Resistant Epilepsy / diagnosis metabolism

来  源:   DOI:10.3390/ijms25126488

Abstract:
A central role for neuroinflammation in epileptogenesis has recently been suggested by several investigations. This systematic review explores the role of inflammatory mediators in epileptogenesis, its association with seizure severity, and its correlation with drug-resistant epilepsy (DRE). The study analysed articles published in JCR journals from 2019 to 2024. The search strategy comprised the MESH, free terms of \"Neuroinflammation\", and selective searches for the following single biomarkers that had previously been selected from the relevant literature: \"High mobility group box 1/HMGB1\", \"Toll-Like-Receptor 4/TLR-4\", \"Interleukin-1/IL-1\", \"Interleukin-6/IL-6\", \"Transforming growth factor beta/TGF-β\", and \"Tumour necrosis factor-alpha/TNF-α\". These queries were all combined with the MESH terms \"Epileptogenesis\" and \"Epilepsy\". We found 243 articles related to epileptogenesis and neuroinflammation, with 356 articles from selective searches by biomarker type. After eliminating duplicates, 324 articles were evaluated, with 272 excluded and 55 evaluated by the authors. A total of 21 articles were included in the qualitative evaluation, including 18 case-control studies, 2 case series, and 1 prospective study. As conclusion, this systematic review provides acceptable support for five biomarkers, including TNF-α and some of its soluble receptors (sTNFr2), HMGB1, TLR-4, CCL2 and IL-33. Certain receptors, cytokines, and chemokines are examples of neuroinflammation-related biomarkers that may be crucial for the early diagnosis of refractory epilepsy or may be connected to the control of epileptic seizures. Their value will be better defined by future studies.
摘要:
一些研究最近提出了神经炎症在癫痫发生中的核心作用。本系统综述探讨了炎症介质在癫痫发生中的作用。它与癫痫发作严重程度的关联,及其与耐药癫痫(DRE)的相关性。该研究分析了2019年至2024年JCR期刊上发表的文章。搜索策略包括MESH,“神经炎症”的免费条款,并选择性搜索先前从相关文献中选择的以下单个生物标志物:“高迁移率组框1/HMGB1”,“Toll样受体4/TLR-4”,“白细胞介素-1/IL-1”,“白细胞介素-6/IL-6”,“转化生长因子β/TGF-β”,和“肿瘤坏死因子-α/TNF-α”。这些查询都与MESH术语“癫痫发生”和“癫痫”相结合。我们发现了243篇与癫痫发生和神经炎症有关的文章,356篇文章来自生物标志物类型的选择性搜索。消除重复项之后,对324篇文章进行了评估,其中272个排除在外,55个由作者评估。共有21篇文章被纳入定性评价,包括18项病例对照研究,2个案例系列,和1个前瞻性研究。作为结论,本系统综述为五种生物标志物提供了可接受的支持,包括TNF-α及其一些可溶性受体(sTNFr2),HMGB1、TLR-4、CCL2和IL-33。某些受体,细胞因子,和趋化因子是神经炎症相关生物标志物的例子,这些生物标志物可能对难治性癫痫的早期诊断至关重要,或者可能与癫痫发作的控制有关.它们的价值将在未来的研究中得到更好的定义。
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