| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 4343546 | Neuroscience Letters | 2014 | 5 Pages |
•Cell survival by rhEpo-intranasal administration in ischemic hippocampus.•Modified expression of Epo and EpoR by ischemia and after rhEpo-intranasal.•Increased phosphorilation of the EpoR by rhEpo administration.
Erythropoietin in the nervous system is a potential neuroprotective factor for cerebral ischemic damage due to specific-binding to the erythropoietin receptor, which is associated with survival mechanisms. However, the role of its receptor is unclear. Thus, this work assessed whether a low dose (500 UI/Kg) of intranasal recombinant human erythropoietin administered 3 h after ischemia induced changes in the activation of its receptor at the Tyr456-phosphorylated site in ischemic hippocampi in rats. The results showed that recombinant human erythropoietin after injury maintained cell survival and was associated with an increase in receptor phosphorylation at the Tyr456 site as an initial signaling step, which correlated with a neuroprotective effect.
