High-mobility group box1 protein promotes neuroinflammation after intracerebral hemorrhage in rats

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• 作者：C. Lei^a ; ^{leichunyan328@163.com} ; S. Lin^a ; ^{wumu8413@163.com} ; C. Zhang^a ; ^{zhangcanfei2003@163.com} ; W. Tao^a ; ^{annietaotao@gmail.com} ; W. Dong^a ; ^{toto.topig@hotmail.com} ; Z. Hao^a ; ^{zhilong1983@126.com} ; M. Liu^a ; ^b ; ^{wyplmh@hotmail.com} ; B. Wu^a ; ^b ; ^{dragonwbtxf@hotmail.com}
• 关键词：BBB ; blood&ndash ; brain barrier ; EP ; ethyl pyruvate ; HMGB1 ; high-mobility group box1 ; ICH ; intracerebral hemorrhage ; RAGE ; receptor for advanced glycation end products ; TLR4 ; toll-like receptor-4 ; TUNEL ; terminal deoxynucleotidyl transferase-mediated dUTP-
• 刊名：Neuroscience
• 出版年：2013
• 出版时间：3 January, 2013
• 年：2013
• 卷：228
• 期：Complete
• 页码：190-199
• 全文大小：1654 K

文摘

High-mobility group box1 (HMGB1) protein is massively released into the cytoplasm and induces inflammation following various insults such as sepsis, acute cerebral ischemia, and pancreatitis. However, whether HMGB1 can act as an early proinflammatory cytokine to promote inflammation after intracerebral hemorrhage (ICH) is unclear. We explored this question using a rat model of collagenase-induced ICH. We found that HMGB1 was released into the cytoplasm soon after ICH. Administration of ethyl pyruvate decreased the level of HMGB1 and microglia around the hematoma. Ethyl pyruvate also ameliorated ICH-induced neuronal apoptosis, cerebral edema, and neurological impairment. These findings suggest that HMGB1 may act as an early proinflammatory cytokine within the neurovascular unit to mediate inflammation during the acute phase of ICH.