科研之友
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摘要
Stroke resulting from cerebral ischemia or haemorrhage is a common cause of the death of neuronal cells and neurological dysfunction in humans. Finding therapeutics to improve outcome from brain ischemic injury has proved to be challenging. The efficacy of neuroprotective compounds identified in experimental brain ischemia models thus far have failed to successfully translate in clinical human trials. Recent experimental evidence indicates that inhibition of zinc-dependent histone deacetylases can protect neuronal and oligodendroglial cells from the damaging effects of ischemic insult, which may contribute to improved functional outcome. In this review we briefly highlight the current data supporting a beneficial role of histone deacetylation in experimental brain ischemia. We also discuss the molecular mechanism of neuroprotection.
- 出版日期2014
