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阐明高迁移率族蛋白B1在蛛网膜下腔出血中的新型生物标志物及治疗潜力:综述

Elucidating the novel biomarker and therapeutic potentials of High-mobility group box 1 in Subarachnoid hemorrhage: A review.

作者信息

Richard Seidu A

机构信息

Department of Medicine, Princefield University, P. O. Box MA 128, Ho-Volta Region, Ghana West Africa.

出版信息

AIMS Neurosci. 2019 Dec 2;6(4):316-332. doi: 10.3934/Neuroscience.2019.4.316. eCollection 2019.

Abstract

Subarachnoid hemorrhage (SAH) frequently arises after an aneurysm in a cerebral artery ruptures, resulting into bleeding as well as clot formation. High-mobility group box 1 (HMGB1) is an extremely preserved, universal protein secreted in the nuclei of all cell varieties. This review explores the biomarker as well as therapeutic potentials of HMBG1 in SAH especially during the occurrence of cerebral vasospasms. Plasma HMGB1 levels have proven to be very useful prognosticators of effective outcome as well as death after SAH. Correspondingly, higher HMGB1 levels in the cerebrospinal fluid (CSF) of SAH patients correlated well with poor outcome; signifying that, CSF level of HMGB1 is a novel predictor of outcome following SAH. Nonetheless, the degree of angiographic vasospasm does not always correlate with the degree of neurological deficits in SAH patients. HMGB1 stimulated cerebral vasospasm, augmented gene as well as protein secretory levels of receptor for advance glycation end product (RAGE) in neurons following SAH; which means that, silencing HMGB1 during SAH could be of therapeutic value. Compounds like resveratrol, glycyrrhizin, rhinacanthin, purpurogallin, 4'-O-β-D-Glucosyl-5-O-Methylvisamminol (4OGOMV) as well as receptor-interacting serine/threonine-protein kinase 3 (RIPK3) gene are capable of interacting with HMGB1 resulting in therapeutic benefits following SAH.

摘要

蛛网膜下腔出血(SAH)常因脑动脉中的动脉瘤破裂而引发,导致出血和血栓形成。高迁移率族蛋白B1(HMGB1)是一种在所有细胞类型的细胞核中分泌的高度保守的通用蛋白。本综述探讨了HMGB1在SAH中的生物标志物及治疗潜力,尤其是在脑血管痉挛发生期间。血浆HMGB1水平已被证明是SAH后有效预后及死亡的非常有用的预测指标。相应地,SAH患者脑脊液(CSF)中较高的HMGB1水平与不良预后密切相关;这表明,CSF中HMGB1水平是SAH后预后的一个新的预测指标。尽管如此,血管造影血管痉挛的程度并不总是与SAH患者的神经功能缺损程度相关。HMGB1刺激脑血管痉挛,增加SAH后神经元中晚期糖基化终产物受体(RAGE)的基因及蛋白分泌水平;这意味着,在SAH期间沉默HMGB1可能具有治疗价值。白藜芦醇、甘草甜素、 rhinacanthin、 紫铆因、4'-O-β-D-葡萄糖基-5-O-甲基维斯阿米醇(4OGOMV)以及受体相互作用丝氨酸/苏氨酸蛋白激酶3(RIPK3)基因等化合物能够与HMGB1相互作用,在SAH后产生治疗益处。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8715/7179354/8a708144341f/neurosci-06-04-316-g001.jpg

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