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Titolo:
Protective effects of 1 alpha,25-(OH)(2)D-3 against the neurotoxicity of glutamate and reactive oxygen species in mesencephalic culture
Autore:
Ibi, M; Sawada, H; Nakanishi, M; Kume, T; Katsuki, H; Kaneko, S; Shimohama, S; Akaike, A;
Indirizzi:
Kyoto Univ, Grad Sch Pharmaceut Sci, Dept Pharmacol, Sakyo Ku, Kyoto 6068501, Japan Kyoto Univ Kyoto Japan 6068501 Pharmacol, Sakyo Ku, Kyoto 6068501, Japan Kyoto Univ, Grad Sch Med, Dept Neurol, Sakyo Ku, Kyoto 6068507, Japan Kyoto Univ Kyoto Japan 6068507 pt Neurol, Sakyo Ku, Kyoto 6068507, Japan Kyoto Univ, Grad Sch Pharmaceut Sci, Dept Neuropharmacol, Sakyo Ku, Kyoto 6068501, Japan Kyoto Univ Kyoto Japan 6068501 pharmacol, Sakyo Ku, Kyoto 6068501, Japan
Titolo Testata:
NEUROPHARMACOLOGY
fascicolo: 6, volume: 40, anno: 2001,
pagine: 761 - 771
SICI:
0028-3908(200105)40:6<761:PEO1AA>2.0.ZU;2-0
Fonte:
ISI
Lingua:
ENG
Soggetto:
VITAMIN-D-RECEPTOR; 1,25-DIHYDROXYVITAMIN D-3; DOPAMINERGIC-NEURONS; NITRIC-OXIDE; CELL-LINE; NEUROTROPHIC FACTOR; PARKINSONS-DISEASE; RAT-BRAIN; MECHANISM; DEATH;
Keywords:
1 alpha,25-(OH)(2)D-3; neuroprotection glutamate; dopaminergic neuron; mesencephalon;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
30
Recensione:
Indirizzi per estratti:
Indirizzo: Akaike, A Kyoto Univ, Grad Sch Pharmaceut Sci, Dept Pharmacol, Sakyo Ku, Kyoto 6068501, Japan Kyoto Univ Kyoto Japan 6068501 Sakyo Ku, Kyoto 6068501, Japan
Citazione:
M. Ibi et al., "Protective effects of 1 alpha,25-(OH)(2)D-3 against the neurotoxicity of glutamate and reactive oxygen species in mesencephalic culture", NEUROPHARM, 40(6), 2001, pp. 761-771

Abstract

This study was undertaken to determine whether 1 alpha,25-dihydroxyvitaminD3 [1 alpha,25-(OH)(2)D-3], an active metabolite of vitamin D, protects dopaminergic neurons against the neurotoxic effects of glutamate and dopaminergic toxins using rat mesecephalic culture. Brief glutamate exposure elicited cytotoxicity in both dopaminergic and non-dopaminergic neurons. Pretreatment, but not co-administration, of 1 alpha ,25-(OH)(2)D-3 protected both types of neurons against the cytotoxicity of glutamate in a concentration- and time-dependent manner. The neuroprotective effect of 1 alpha ,25-(OH)(2)D-3 was inhibited by the protein synthesis inhibitor, cycloheximide. To investigate the mechanisms of these neuroprotective effects, we examined the effects of 1 alpha .25-(OH)(2)D-3 on neurotoxicity induced by calcium ionophore and reactive oxygen species (ROS). Pretreatment with 1 alpha ,25-(OH)(2)D-3 protected both types of neurons against the cytotoxicity induced by A23187 in a concentration-dependent manner. Furthermore, 24-h pretreatment with 1 alpha .25-(OH)(2)D-3 concentration-dependently protected both types ofneurons from ROS-induced cytotoxicity. A 24-h incubation with 1 alpha ,25-(OH)(2)D-3 inhibited the increase in intracellular ROS level following H2O2exposure. A 24-h exposure to 1-methyl-4-phenylpyridium ion (MPP+) or 6-hydroxydopamine (6-OHDA) exerted selective neurotoxicity on dopaminergic neurons, and these neurotoxic effects were ameliorated by 1 alpha -25-(OH)(2)D-3. These results suggest that 1 alpha ,25-(OH)(2)D-3 provides protection of dopaminergic neurons against cytotoxicity induced by glutamate and dopaminergic toxins by facilitating cellular functions that reduce oxidative stress. (C) 2001 Elsevier Science Ltd. All rights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 02/10/20 alle ore 01:41:00