Possibility of treatment for brain hemorrhage in acute phase, Elucidation of involvement of protein HMGB1 in all three types of stroke
April 10(Mon), 2017
A research group led by Masahiro Nishibori, Professor at Department of Pharmacology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University has found that High Mobility Group Box-1 (HMGB1) protein, which is released from neuronal cells in response to hematoma, is involved in the mechanism of brain tissue damage following intracerebral hemorrhage. This study was reported in the U.K.’s journal Scientific Reports on April 10.
Strokes are categorized into three types: cerebral infarction, subarachnoid hemorrhage, and intracerebral hemorrhage. The research group carefully observed the action of HMGB1 in a rat model for intracerebral hemorrhage. As a result, they found that HMGB1 (a nuclear protein released from neuronal cells) promotes breakdown of the blood-brain barrier* and induces production of proinflammatory cytokines*. They also found that an anti-HMGB1 antibody, known to neutralize HMGB1 action, reduces the release of HMGB1 and exhibits anti-inflammatory action so that neuronal cell death and paralytic symptoms are reduced. It was also found that some effects are still obtained from the anti-HMGB1 antibody therapy when initiated 3 hours after intracerebral hemorrhage.
Intracerebral hemorrhage is related to high mortality compared to other strokes, and re-occurrence is quite severe. However, there has been no drug developed for reducing nerve damage caused by intracerebral hemorrhage. The anti-HMGB1 antibody therapy is promising and expected to be studied further for practical use.
Journal: Scientific Reports
Title: Anti-high mobility group box-1 (HMGB1) antibody inhibits hemorrhage-induced brain injury and improved neurological deficits in rats.
Year Publication: April, 2017
Okayama University Silicon Valley Office (OUSVO)
|Contact:||Mototaka Senda, Ph.D.|
- brain hemorrhage, HMGB1, anti-HMGB1 antibody therapy