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Titolo:
cAMP potentiates beta-amyloid-induced nitric oxide release from microglia
Autore:
Pyo, H; Jou, I; Jung, S; Joe, E;
Indirizzi:
Ajouuthiv, Sch Med, Dept Pharmacol, Paldal Gu, Suwon 442749, Kyunggi Do, So Ajou Univ Suwon Kyunggi Do South Korea 442749 uwon 442749, Kyunggi Do, So
Titolo Testata:
NEUROREPORT
fascicolo: 1, volume: 10, anno: 1999,
pagine: 37 - 40
SICI:
0959-4965(19990118)10:1<37:CPBNOR>2.0.ZU;2-X
Fonte:
ISI
Lingua:
ENG
Soggetto:
CYCLIC-AMP; ALZHEIMERS-DISEASE; SYNTHASE; GENE; EXPRESSION; INHIBITION; ACTIVATION; FORSKOLIN; ISCHEMIA; PROTEIN;
Keywords:
beta-amyloid peptide; cAMP; microglia; nitric oxide;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
20
Recensione:
Indirizzi per estratti:
Indirizzo: Joe, E Ajou42749, Sch Med, Dept Pharmacol, Paldal Gu, San 5 Woncheon Dong,Suwon 4 Ajou Univ San 5 Woncheon Dong Suwon Kyunggi Do South Korea 442749 4
Citazione:
H. Pyo et al., "cAMP potentiates beta-amyloid-induced nitric oxide release from microglia", NEUROREPORT, 10(1), 1999, pp. 37-40

Abstract

THE beta-amyloid peptide (A beta) has been known to activate microglia andto induce release of nitric oxide (NO). In this study, we examined the effect of cAMP on A beta-induced microglial activation using cultured rat brain microglia. Dibutyryl-cAMP (dbcAMP) and 3-isobutyl-1-methylxanthine (IBMX)significantly potentiated A beta(25-35)- or A beta(1-42)-induced NO release in a dose-dependent manner. The increase in NO release was due to the increased expression of inducible nitric oxide synthase (iNOS). However, forskolin, an adenylate cyclase activator, weakly increased NO release at 10-50 mu M but caused a decrease at 100 mu M. These results suggest that increasein intracellular cAMP could potentiate microglial activation induced by A beta. (C) 1999 Lippincott Williams & Wilkins.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 20/09/20 alle ore 10:38:06