Novel synthetic analogue of ACTH 4–10 (Semax) but not glycine prevents the enhanced nitric oxide generation in cerebral cortex of rats with incomplete global ischemia

• Published in: Brain research 2001-03, Vol.894 (1), p.145-149
• Main Authors: Bashkatova, Valentina G, Koshelev, Vladimir B, Fadyukova, Olga E, Alexeev, Alexandr A, Vanin, Anatolii F, Rayevsky, Kirill S, Ashmarin, Igor P, Armstrong, David M
• Format: Article
• Language: English
• Subjects: Adrenocorticotropic Hormone - analogs & derivatives; Adrenocorticotropic Hormone - chemistry; Adrenocorticotropic Hormone - pharmacology; Animals; Brain Ischemia - metabolism; Cerebral Cortex - drug effects; Cerebral Cortex - metabolism; Electron paramagnetic resonance spectroscopy; Global ischemia; Glycine - pharmacology; Lipid peroxidation; Lipid Peroxidation - drug effects; Lipid Peroxidation - physiology; Male; Nitric oxide (NO); Nitric Oxide - metabolism; Nootropic Agents - pharmacology; Peptide Fragments - chemistry; Peptide Fragments - pharmacology; Rats; Rats, Wistar; Semax
• ISSN: 0006-8993; 1872-6240
• DOI: 10.1016/S0006-8993(00)03324-2

This work investigates whether nitric oxide production and lipid peroxidation contribute to the pathophysiology of ischemia and whether glycine and a novel Russian compound, Semax are neuroprotective via a mechanism involving the regulation nitric oxide (NO) and lipid peroxidation. In brief, nitric oxide and indices of lipid peroxidation were elevated following global ischemia. While glycine proved ineffective in reducing NO levels or ameliorating the neurological deficits following global ischemia, Semax proved to be highly effective in abating the rise in nitric oxide and restoring neurologic functioning.