http://tan.sagepub.com/content/5/3/161.abstract?etoc
Abstract
Acute stroke is one of the major causes of
death and disabilities. Since the 1980s many clinical studies have been
conducted
to evaluate neuroprotective approaches to treat
this important brain vascular event. However, to date the only drug
approved
(recombinant tissue plasminogen activator [rtPA])
represents a thrombolytic, nonneuroprotective approach. An important
neuroprotective
strategy is based on erythropoietin (EPO).
Exogenously administered EPO exhibits neuroprotective effects in
numerous animal
models, through the activation of anti-apoptotic,
anti-oxidant and anti-inflammatory pathways as well as through the
stimulation
of angiogenic and neurogenic events. The capability
of EPO to cross the blood–brain barrier after systemic administration
and its effective therapeutic window are advantages
for human acute stroke therapy. However, a multicenter stroke trial
where
recombinant human EPO (rhEPO) was combined with
rtPA had negative outcomes. The present paper reviews the EPO
neuroprotective
strategy and its mechanisms in ischemic stroke and
in other human nervous system diseases.
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