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Growth hormone-releasing peptide hexarelin reduces neonatal brain injury and alters Akt/glycogen synthase kinase-3beta phosphorylation

Artikel i vetenskaplig tidskrift
Författare Katarina Gustafsson Brywe
Anna-Lena Leverin
Malin Gustavsson
Carina Mallard
Riccarda Granata
S. Destefanis
Marco Volante
Henrik Hagberg
Ezio Ghigo
Jörgen Isgaard
Publicerad i Endocrinology
Volym 146
Nummer/häfte 11
Sidor 4665-72
Publiceringsår 2005
Publicerad vid Institutionen för kvinnors och barns hälsa, Avdelningen för obstetrik och gynekologi
Institutionen för invärtesmedicin
Institutionen för fysiologi och farmakologi, Avdelningen för fysiologi
Sidor 4665-72
Språk en
Länkar www.ncbi.nlm.nih.gov/entrez/query.f...
Ämnesord Animals, Animals, Newborn, Brain Ischemia/metabolism/*pathology, Caspase 3, Caspases/antagonists & inhibitors, Female, Glycogen Synthase Kinase 3/*metabolism, Growth Hormone/metabolism, Hypoxia, Brain/metabolism/*pathology, Immunohistochemistry, Insulin-Like Growth Factor I/metabolism, Male, Neuroprotective Agents/*pharmacology, Oligopeptides/*pharmacology, Phosphorylation/drug effects, Rats, Rats, Wistar, Receptor, IGF Type 1/metabolism
Ämneskategorier Medicin och Hälsovetenskap

Sammanfattning

Hexarelin (HEX) is a peptide GH secretagogue with a potent ability to stimulate GH 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 HEX on the central nervous system 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 HEX treatment was administered intracerebroventricularly, 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 group, 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-3beta, whereas ERK was unaffected. In conclusion, we demonstrate for the first time that HEX is neuroprotective in the neonatal setting in vivo and that increased Akt signaling is associated with downstream attenuation of glycogen synthase kinase-3beta activity and caspase-dependent cell death.

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