Effect of L-carnitine on postischemic inhibition of protein synthesis in the rat brain

• Published in: General physiology and biophysics 2009-09, Vol.28 (3), p.242-248
• Main Authors: Burda, Jozef, Hernández Viadel, Mariluz, Danielisová, Viera, Némethová, Miroslava, Montoliu, Carmina, Felipo, Vicente
• Format: Article
• Language: English
• Subjects: Animals; Brain - drug effects; Brain - metabolism; Brain Ischemia - drug therapy; Brain Ischemia - metabolism; Carnitine - administration & dosage; Carnitine - pharmacology; Cerebral Cortex - drug effects; Cerebral Cortex - metabolism; Corpus Striatum - drug effects; Corpus Striatum - metabolism; Hippocampus - drug effects; Hippocampus - metabolism; Nerve Degeneration - drug therapy; Nerve Degeneration - metabolism; Neurons - drug effects; Neurons - metabolism; Neuroprotective Agents - administration & dosage; Neuroprotective Agents - pharmacology; Protein Biosynthesis - drug effects; Rats; Rats, Wistar; Reperfusion Injury - drug therapy; Reperfusion Injury - metabolism; Time Factors
• ISSN: 0231-5882
• DOI: 10.4149/gpb_2009_03_242

The purpose of this study was to investigate effects of carnitine administration on protein synthesis recovery after transient cerebral ischemia. Rats received L-carnitine in two doses of 16 mmol/kg i.p. 15 min before ischemia and just on the onset of reperfusion. Transient forebrain ischemia was induced by 4-vessel occlusion for 15 min, followed by 30 min or 7 days of reperfusion. Protein synthesis rate, reinitiation ability and neurodegeneration in the frontal cortex and hippocampus were measured by the incorporation of radioactively labelled leucine into polypeptide chains in postmitochondrial supernatants and by Fluoro-Jade B staining. A protective effect was observed, on protein synthesis as well as the number of surviving neurons, in the L-carnitine-treated groups. Our results indicate that L-carnitine can exert a protective effect in the development of reperfusion-induced injury. L-carnitine significantly reduced the ischemia/reperfusion-induced inhibition of translation and neurodegeneration in the neocortex as well as in the highly sensitive hippocampus and dorsolateral striatum. We expect that the ability of L-carnitine to keep translational machinery on facilitates efficacy of postischemic remodulation of gene expression.