Neuropharmacology And NeurotoxicologyBaicalein protects cortical neurons from β-amyloid (25-35) induced toxicityLebeau, AntonyCA; Esclaire, Françoise1; Rostène, William; Pélaprat, DidierAuthor Information INSERM U 339, Hôpital Saint-Antoine, 184 rue du Faubourg Saint-Antoine 75571 Paris Cedex 12; 1Laboratoire d'Histologie et Biologie Cellulaire, Unité de Neurobiologie Cellulaire, Faculté de Médecine 87025 Limoges, France CACorresponding Author Received 25 April 2001; accepted 10 May 2001 Neuroreport: July 20, 2001 - Volume 12 - Issue 10 - p 2199-2202 Buy Abstract Accumulation of amyloid β peptide (Aβ) 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 Aβ on rat cortical cells. The 12-lipoxygenase inhibitor baicalein attenuated both neuronal apoptosis and c-jun protein over-expression induced by Aβ(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 Aβ(25-35), and that specific 12-lipoxygenase inhibitors might be of interest in AD. © 2001 Lippincott Williams & Wilkins, Inc.