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Titolo:
Dexanabinol (HU-211): A nonpsychotropic cannabinoid with neuroprotective properties
Autore:
Shohami, E; Mechoulam, R;
Indirizzi:
Hebrew Univ Jerusalem, Sch Pharm, Dept Pharmacol, IL-91120 Jerusalem, Israel Hebrew Univ Jerusalem Jerusalem Israel IL-91120 -91120 Jerusalem, Israel Hebrew Univ Jerusalem, Sch Pharm, Dept Med Chem, IL-91120 Jerusalem, Israel Hebrew Univ Jerusalem Jerusalem Israel IL-91120 -91120 Jerusalem, Israel
Titolo Testata:
DRUG DEVELOPMENT RESEARCH
fascicolo: 3-4, volume: 50, anno: 2000,
pagine: 211 - 215
SICI:
0272-4391(200007/08)50:3-4<211:D(ANCW>2.0.ZU;2-I
Fonte:
ISI
Lingua:
ENG
Soggetto:
CLOSED-HEAD INJURY; TUMOR-NECROSIS-FACTOR; NONCOMPETITIVE NMDA ANTAGONIST; BRAIN-DAMAGE; RECEPTOR ANTAGONIST; SEPTIC SHOCK; OPTIC-NERVE; RAT; ISCHEMIA; MECHANISMS;
Keywords:
dexanabinol; NMDA-antagonist; TNF-inhibitor; brain injury; stroke;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
34
Recensione:
Indirizzi per estratti:
Indirizzo: Shohami, E Hebrew Univ Jerusalem, Sch Pharm, Dept Pharmacol, IL-91120 Jerusalem, Israel Hebrew Univ Jerusalem Jerusalem Israel IL-91120 salem, Israel
Citazione:
E. Shohami e R. Mechoulam, "Dexanabinol (HU-211): A nonpsychotropic cannabinoid with neuroprotective properties", DRUG DEV R, 50(3-4), 2000, pp. 211-215

Abstract

The synthetic cannabinoid (+)-(6aS,10aS)-11-hydroxy-Delta-8-tetrahydrocannabinol 1',1'dimethylheptyl (dexanabinol, HU-211) is inactive as a cannabimimetic, but exhibits pharmacological properties characteristic of an N-methyl-D-aspartate (NMDA)-receptor antagonist. It blocks NMDA-receptors stereospecifically by interacting with a site close to, but distinct from, that of uncompetitive NMDA-receptor antagonists and from the recognition sites of glutamate, glycine, and polyamines. HU-211 inhibits the synthesis of tumor necrosis factor alpha (TNF alpha) and possesses antioxidant properties. HU-211 blocked NMDA-induced Ca-45 uptake by primary neuronal cultures of rat forebrain and protected the same neuronal cultures against NMDA and glutamateneurotoxicity. Moreover, HU-211 effectively scavenged peroxy radicals in vitro and protected cultured neurons from the toxic effects of reactive oxygen species (ROS). In addition, HU-211 markedly suppressed in vitro TNF alpha production and nitric oxide (NO) generation (by > 90%) by both murine peritoneal macrophages and rat alveolar macrophage cell line exposed to lipopolysaccharide (LPS). Since glutamate, ROS and TNF alpha. are implicated in the pathophysiology of various acute conditions, the promising results showing neuroprotection by HU-211, acting via multiple mechanisms, led to a series of studies in which the drug was given to experimental animals. In the present review we discuss results from experiments describing the potential use of HU-211 as a neuroprotective agent in models of traumatic brain injury, stroke, optic nerve injury, pneumacocal meningitis, sepsis, and soman toxicity. In addition, HU-211 was introduced into clinical trials for traumatic brain injury and the successful results of two phases of clinical trialsin head injured patients are also shown. Drug Dev. Res. 50:211-215, 2000. (C) 2000 Wiley-Liss, Inc.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 20/01/20 alle ore 04:39:46