論文

査読有り 筆頭著者
2017年5月

Protection of the Blood-Brain Barrier as a Therapeutic Strategy for Brain Damage

BIOLOGICAL & PHARMACEUTICAL BULLETIN
  • Shotaro Michinaga
  • ,
  • Yutaka Koyama

40
5
開始ページ
569
終了ページ
575
記述言語
英語
掲載種別
DOI
10.1248/bpb.b16-00991
出版者・発行元
PHARMACEUTICAL SOC JAPAN

Severe brain damage by trauma, ischemia, and hemorrhage lead to fatal conditions including sudden death, subsequent complications of the extremities and cognitive dysfunctions. Despite the urgent need for treatments for these complications, currently available therapeutic drugs are limited. Blood brain barrier (BBB) disruption is a common pathogenic feature in many types of brain damage. The characteristic pathophysiological conditions caused by BBB disruption are brain edema resulting from an excessive increase of brain water content, inflammatory damage caused by infiltrating immune cells, and hemorrhage caused by the breakdown of microvessel structures. Because these pathogenic features induced by BBB disruption cause fatal conditions, their improvement is a desirable strategy. Many studies using experimental animal models have focused on molecules involved in BBB disruption, including vascular endothelial growth factors (VEGFs), matrix metalloproteinases (MM Ps) and endothelins (ETs). The inhibition of these factors in several experimental animals was protective against BBB disruption caused by several types of brain damage, and ameliorated brain edema, inflammatory damage, and hemorrhagic transformation. In patients with brain damage, the up-regulation of these factors was observed and was related to brain damage severity. Thus, BBB protection by targeting VEGFs, MMPs, and ETs might be a novel strategy for the treatment of brain damage.

リンク情報
DOI
https://doi.org/10.1248/bpb.b16-00991
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000400319100006&DestApp=WOS_CPL
ID情報
  • DOI : 10.1248/bpb.b16-00991
  • ISSN : 0918-6158
  • Web of Science ID : WOS:000400319100006

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