Post-ischemic activation of protein kinase C ε protects the hippocampus from cerebral ischemic injury via alterations in cerebral blood flow.
Neurosci Lett
; 487(2): 158-62, 2011 Jan 07.
Article
in En
| MEDLINE
| ID: mdl-20951185
ABSTRACT
Protein kinase C (PKC) is a family of serine/threonine-isozymes that are involved in many signaling events in normal and disease states. Previous studies from our lab have demonstrated that ÉPKC plays a pivotal role in neuroprotection induced by ischemic preconditioning. However, the role of ÉPKC during and after brain ischemia is not clearly defined. Therefore, in the present study, we tested the hypothesis that activation of ÉPKC during an ischemic event is neuroprotective. Furthermore, other studies have demonstrated that ÉPKC mediates cerebral ischemic tolerance in the rat brain by decreasing vascular tone. Thus, we also tested the effects of ÉPKC activation during ischemia on cerebral blood flow (CBF). We found that ψÉ-Receptors for Activated C Kinase (RACK), a ÉPKC-selective peptide activator, injected intravenously 30min before induction of global cerebral ischemia conferred neuroprotection in the CA1 region of the rat hippocampus. Moreover, measurements of CBF before, during, and after cerebral ischemia revealed a significant reduction in the reperfusion phase of rats pretreated with ψÉRACK as compared to Tat peptide (vehicle). Our results suggest that ÉPKC can protect the rat brain against ischemic damage by regulating CBF. Thus, ÉPKC may be one of the treatment modalities against ischemic injury.
Full text:
1
Database:
MEDLINE
Main subject:
Brain Ischemia
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Cerebrovascular Circulation
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Neuroprotective Agents
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Protein Kinase C-epsilon
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Hippocampus
Limits:
Animals
Language:
En
Year:
2011
Type:
Article