Extracellular signal‐regulated kinase (ERK) 1/2 is activated during acute phase of stroke and contributes to stroke pathology. We have found that acute treatment with MEK1/2 inhibitors decreases infarct size and… Click to show full abstract
Extracellular signal‐regulated kinase (ERK) 1/2 is activated during acute phase of stroke and contributes to stroke pathology. We have found that acute treatment with MEK1/2 inhibitors decreases infarct size and neurological deficits 2 days after experimental stroke. However, it is not known whether benefits of this inhibition persist long‐term. Therefore, the aim of this study was to assess neurological function, infarct size and recovery processes 14 days after stroke in male rats to determine long‐term outcome following acute treatment with the MEK1/2 inhibitor U0126.
               
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