論文

国際誌
2019年2月

Anti-High Mobility Group Box 1 Antibody Therapy May Prevent Cognitive Dysfunction After Traumatic Brain Injury.

World neurosurgery
  • Yu Okuma
  • ,
  • Hidenori Wake
  • ,
  • Kiyoshi Teshigawara
  • ,
  • Yu Takahashi
  • ,
  • Tomohito Hishikawa
  • ,
  • Takao Yasuhara
  • ,
  • Shuji Mori
  • ,
  • Hideo K Takahashi
  • ,
  • Isao Date
  • ,
  • Masahiro Nishibori

122
開始ページ
e864-e871
終了ページ
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1016/j.wneu.2018.10.164

BACKGROUND: High mobility group box 1 (HMGB1) protein plays a key role in triggering inflammatory responses in many diseases. Our previous study showed that HMGB1 is found upstream of secondary damage in traumatic brain injury (TBI). We found that anti-HMGB1 monoclonal antibody (mAb) effectively decreased acute brain damage, including the disruption of the blood-brain barrier, brain edema, and neurologic dysfunction. This effect of anti-HMGB1 mAb lasts for at least 1 week. In this study, we explored subacute effects of anti-HMGB1 mAb after TBI. METHODS: TBI was induced in rats by fluid percussion. Anti-HMGB1 mAb or control mAb was given intravenously after TBI. Histochemical staining, plasma levels of HMGB1, motor activity and memory, and video electroencephalography monitoring were evaluated 2 weeks after fluid percussion injury. RESULTS: Anti-HMGB1 mAb remarkably attenuated accumulation of activated microglia in the rat cortex in the ipsilateral hemisphere after TBI. Anti-HMGB1 mAb also prevented neuronal death in the hippocampus in the ipsilateral hemisphere after TBI. Treatment of rats with anti-HMGB1 mAb inhibited HMGB1 translocation and suppressed impairment of motor function. The beneficial effects of anti-HMGB1 mAb on motor and cognitive function persisted for 14 days after injury. Treatment with anti-HMGB1 mAb also had positive effects on electroencephalography activity. CONCLUSIONS: The beneficial effects of anti-HMGB1 mAb continued during the subacute postinjury phase, suggesting that anti-HMGB1 mAb may prevent cognitive dysfunction after TBI.

リンク情報
DOI
https://doi.org/10.1016/j.wneu.2018.10.164
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/30391757
ID情報
  • DOI : 10.1016/j.wneu.2018.10.164
  • PubMed ID : 30391757

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