Baicalein protects cortical neurons from beta-amyloid (25-35) induced toxicity
Autor: | Antony Lebeau, William Rostène, Didier Pélaprat, Francoise Esclaire |
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Rok vydání: | 2001 |
Předmět: |
Amyloid
Amyloid beta Proto-Oncogene Proteins c-jun Inflammation Apoptosis Pharmacology Lipoxygenase chemistry.chemical_compound mental disorders medicine Animals Masoprocol Rats Wistar Cells Cultured Cerebral Cortex Flavonoids Neurons Amyloid beta-Peptides biology General Neuroscience Neurodegeneration Free Radical Scavengers medicine.disease Embryo Mammalian Peptide Fragments Baicalein Rats Nordihydroguaiaretic acid Neuroprotective Agents Biochemistry chemistry Flavanones biology.protein medicine.symptom |
Zdroj: | Neuroreport. 12(10) |
ISSN: | 0959-4965 |
Popis: | Accumulation of amyloid beta peptide (Abeta) has been suggested to contribute to neurodegeneration in Alzheimer's disease (AD). Since chronic inflammation occurs in AD pathogenesis and lipoxygenases are important mediators of inflammatory processes, we evaluated the effect of lipoxygenase inhibitors on apoptosis induced by Abeta on rat cortical cells. The 12-lipoxygenase inhibitor baicalein attenuated both neuronal apoptosis and c-jun protein over-expression induced by Abeta(25- 35), whereas no protection was found with the broad spectrum lipoxygenase inhibitor nordihydroguaiaretic acid or the 5-lipoxygenase inhibitor caffeic acid. These results suggest that 12-lipoxygenase participates in a c-jun-dependent apoptosis pathway triggered by Abeta(25-35), and that specific 12-lipoxygenase inhibitors might be of interest in AD. |
Databáze: | OpenAIRE |
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