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2014 Fiscal Year Final Research Report

Drug development for brain and spinal cord trauma targeting HMGB1

Research Project

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Project/Area Number 24390061
Research Category

Grant-in-Aid for Scientific Research (B)

Allocation TypePartial Multi-year Fund
Section一般
Research Field General pharmacology
Research InstitutionOkayama University

Principal Investigator

NISHIBORI Masahiro  岡山大学, 医歯(薬)学総合研究科, 教授 (50135943)

Co-Investigator(Kenkyū-buntansha) DATE Isao  岡山大学, 大学院医歯薬学総合研究科, 教授 (70236785)
TAKAHASI Hideo  近畿大学, 医学部, 教授 (60335627)
RYU Katsuyaku  岡山大学, 大学院医歯薬学総合研究科, 助教 (40432637)
WAKE Hidenori  岡山大学, 大学院医歯薬学総合研究科, 助教 (60570520)
TESHIGAWARA Kiyoshi  岡山大学, 大学院医歯薬学総合研究科, 助教 (40403737)
Project Period (FY) 2012-04-01 – 2015-03-31
KeywordsHMGB1 / 脳外傷 / グリチルリチン / 脊髄損傷 / 血液脳関門 / ミクログリア
Outline of Final Research Achievements

Fluid-percussion-induced injury on the brain was produced in rats. The increase in blood-brain barrier permeability and resulting brain edema was detected in the penumbra area. The HMGB1 translocation from nuclei to extracellular space was observed in neurons in injured region. BBB disruption, activation of microglia, and the increase in the expression of inflammatory cytokines were observed in the same region. The treatment with anti-HMGB1 mAb inhibited the inflammatory response induced by injury by 85%, associated with the improvement of neurological symptoms. Glycyrrhizin, an active constituent of licorice that binds to HMGB1, produced a similar activity to anti-HMGB1 mAb. The inhibitory effects of glycyrrhizin on traumatic brain injury was not observed in RAGE knockout mice, suggesting the involvement of RAGE in the action of HMGB1 released from neurons. Similarly, anti-HMGB1 mAb improved the paralysis of hind limb dramatically due to the prevention of blood-spinal cord barrier.

Free Research Field

医学(薬理学)

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Published: 2016-06-03  

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