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Titolo:
Cilostazol, a cyclic AMP phosphodiesterase inhibitor, stimulates nitric oxide production and sodium potassium adenosine triphosphatase activity in SH-SY5Y human neuroblastoma cells
Autore:
Inada, H; Shindo, H; Tawata, M; Onaya, T;
Indirizzi:
Yamanashi Med Univ, Dept Internal Med 3, Yamanashi 4093898, Japan Yamanashi Med Univ Yamanashi Japan 4093898 d 3, Yamanashi 4093898, Japan
Titolo Testata:
LIFE SCIENCES
fascicolo: 13, volume: 65, anno: 1999,
pagine: 1413 - 1422
SICI:
0024-3205(19990820)65:13<1413:CACAPI>2.0.ZU;2-U
Fonte:
ISI
Lingua:
ENG
Soggetto:
EXPERIMENTAL DIABETIC NEUROPATHY; DEPENDENT PROTEIN-KINASE; SMOOTH-MUSCLE CELLS; ALDOSE REDUCTASE; PERIPHERAL-NERVE; RATS; NA+; ADENOSINE-3',5'-MONOPHOSPHATE; GMP;
Keywords:
cilostazol; nitric oxide; cyclic AMP; protein kinase A; sodium potassium ATPase activity; SH-SY5Y cell; diabetic neuropathy;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
26
Recensione:
Indirizzi per estratti:
Indirizzo: Shindo, H Yamanashi Med Univ, Dept Internal Med 3, Yamanashi 4093898, Japan Yamanashi Med Univ Yamanashi Japan 4093898 ashi 4093898, Japan
Citazione:
H. Inada et al., "Cilostazol, a cyclic AMP phosphodiesterase inhibitor, stimulates nitric oxide production and sodium potassium adenosine triphosphatase activity in SH-SY5Y human neuroblastoma cells", LIFE SCI, 65(13), 1999, pp. 1413-1422

Abstract

Deficiencies in cellular cyclic AMP (cAMP) and nitric oxide (NO) production are thought to be involved in the pathogenesis of diabetic neuropathy. Weused a human neuroblastoma cell line, SH-SY5Y, to investigate the effect of cilostazol, a specific cAMP phosphodiesterase inhibitor, on NO productionand Na+, K+-ATPase activity. SH-SY5Y cells were cultured under 5 or 50 mM glucose for 5-6 days, the cells were then exposed to cilostazol or other chemicals and nitrite, cAMP and Na+, K+-ATPase activity were measured. In cells grown in 50 mM glucose, cilostazol was observed to increase significantly both NO production and cellular cAMP accumulation in a time and dose-dependent manner. Cilostazol also significantly recovered reduced levels:of:protein kinase A activity (PKA) in 50 mM glucose. Furthermore, a PKA inhibitor, H-89 significantly suppressed the increase in NO production stimulated bycilostazol, suggesting that cilostazol stimulates NO production by activating PKA. Cilostazol did not affect either sorbitol or myo-inositol concentrations. Dexamethazone, which is known to induce inducible NO synthase, had no effect on NO production stimulated by cilostazol, suggesting that cilostazol stimulates NO production catalyzed by neuronal constitutive NO synthase (ncNOS) in SH-SY5Y cells. L-arginine, which is an NO agonist enhanced Na+, K+-ATPase activity in cells grown in 50 mM glucose, NG-nitro-L-arginine methyl ester (L-NAME), which is an NOS inhibitor inhibited basal Na+, K+-ATPase activity in 5 mM glucose and suppressed the increased enzyme activity induced by cilostazol in 50 mM glucose. The above results confirmed our previous observation that NO regulates Naf, K+-ATPase activity in SH-SY5Y cellsand suggest that cilostazol increases Na+, KC-ATPase activity, at least inpart, by stimulating NO production. The present results also suggest that cilostazol has a beneficial effect on diabetic neuropathy by improving Na+,K+-ATPase activity via directly increasing cAMP and NO production in nerves.

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Documento generato il 30/09/20 alle ore 09:41:42