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Submitted on April 4, 2005
Accepted on July 29, 2005
phosphorylation
Department of Obstetrics and Gynecology, Perinatal Center, Sahlgrenska Academy, Göteborg, Sweden; Department of Physiology and Pharmacology, Sahlgrenska Academy, Göteborg, Sweden; Department of Internal Medicine University of Turin, Turin, Italy; Department of Biomedical Sciences & Oncology, University of Turin, Turin, Italy; Research Center for Endocrinology and Metabolism, Department of Internal Medicine Sahlgrenska Academy, Göteborg, Sweden
* To whom correspondence should be addressed. E-mail: katarina.g.brywe{at}medfak.gu.se.
Hexarelin is a peptide growth hormone secretagogue with a potent ability to stimulate growth hormone secretion and recently reported cardioprotective actions. However, its effects in the brain are largely unknown and the aim of the present study was to examine the potential protective effect of hexarelin on the CNS after injury, as well as on caspase-3, Akt and extracellular signal regulated protein kinase (ERK) signaling cascades in a rat model of neonatal hypoxia-ischemia.
Hypoxic-ischemic insult was induced by unilateral carotid ligation and hypoxic exposure (7.7% oxygen) and hexarelin treatment was administered intracerebroventricularly (i.c.v). directly after the insult. Brain damage was quantified at four coronal levels and by regional neuropathological scoring. Brain damage was reduced by 39% in the treatment group compared with vehicle and injury was significantly reduced in the cerebral cortex, hippocampus and thalamus but not in the striatum. The cerebroprotective effect was accompanied by a significant reduction of caspase-3 activity and an increased phosphorylation of Akt and glycogen synthase kinase-3 
(GSK3), whereas ERK was unaffected. In conclusion, we demonstrate for the first time that hexarelin is neuroprotective in the neonatal setting in vivo and that increased Akt signaling was associated with downstream attenuation of GSK3 ctivity and caspase-dependent cell death.
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