Carnosine protects neurons against oxidative stress and modulates the time profile of MAPK cascade signaling
| Autor: | Ekaterina Lakonsteva, Mikhail Krasavin, L. V. Karpova, Konstantin Y. Kulebyakin, Alexander A. Boldyrev |
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| Rok vydání: | 2011 |
| Předmět: |
MAPK/ERK pathway
Cell Survival MAP Kinase Signaling System Clinical Biochemistry Excitotoxicity Carnosine Biology MAPK cascade medicine.disease_cause Biochemistry Neuroprotection chemistry.chemical_compound Cerebellum medicine Animals Rats Wistar Extracellular Signal-Regulated MAP Kinases Homocysteine Cells Cultured Kinase Organic Chemistry JNK Mitogen-Activated Protein Kinases Cell biology Rats Oxidative Stress chemistry Oxidative stress Intracellular |
| Zdroj: | Amino acids. 43(1) |
| ISSN: | 1438-2199 |
| Popis: | Carnosine is a known protector of neuronal cells against oxidative injury which prevents both apoptotic and necrotic cellular death. It was shown earlier that carnosine serves as an intracellular buffer of free radicals. Using the model of ligand-dependent oxidative stress in neurons, we have shown that homocysteine (HC) initiates long-term activation of extracellular signal regulated kinase, isoforms 1 and 2 (ERK 1/2) and Jun N-terminal kinase (JNK) which corresponds to exitotoxic effect resulting in cellular death. l-Carnosine (β-alanyl-l-histidine) protects neurons from both excitotoxic effect of homocysteine and cellular death. Its analogs, β-alanyl-d-histidine (d-carnosine) and l-histidyl-β-alanine, restricted accumulation of free radicals and delayed activation of ERK1/2 and JNK in neuronal cells, but did not promote neuronal viability. |
| Databáze: | OpenAIRE |
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