Protective Actions of Ghrelin on Global Cerebral Ischemia-Induced Memory Deficits
NEUROPHYSIOLOGY, cilt.46, sa.4, ss.343-351, 2014 (SCI-Expanded, Scopus)
- Yayın Türü: Makale / Tam Makale
- Cilt numarası: 46 Sayı: 4
- Basım Tarihi: 2014
- Doi Numarası: 10.1007/s11062-014-9454-1
- Dergi Adı: NEUROPHYSIOLOGY
- Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
- Sayfa Sayıları: ss.343-351
- Anahtar Kelimeler: transient global cerebral ischemia, ghrelin, hippocampus, caspase-3, total oxidant status, nitric oxide, NITRIC-OXIDE SYNTHASE, TRANSIENT FOREBRAIN ISCHEMIA, HIPPOCAMPAL DAMAGE, OXIDATIVE STRESS, RAT HIPPOCAMPUS, BRAIN ISCHEMIA, APOPTOSIS, INJURY, MODEL, EXPRESSION
- Açık Arşiv Koleksiyonu: AVESİS Açık Erişim Koleksiyonu
- Akdeniz Üniversitesi Adresli: Evet
Özet
In our study, we investigated transient global cerebral ischemia (TGCI)-induced changes in spatial memory and motor activity together with apoptotic, oxidant, and NO/NOS signaling parameters in rats and the effects of treatment of animals with ghrelin. The TGCI-induced deficiencies of spatial memory and motor activity in the Y-maze and open field tests were attenuated by ghrelin treatment. Furthermore, ghrelin administration lowered the levels of caspase-3 and iNOS elevated by TGCI in the hippocampus. Thus, we conclude that ghrelin exerts a neuroprotective action against hippocampal TGCI injury via influencing apoptotic, oxidant, and/or NO/NOS pathways. If the underlying mechanisms of action of this agent are fully clarified, ghrelin might be a candidate drug for treatment of TGCI-induced memory impairments.