Dexmedetomidine attenuates lipopolysaccharide-induced proinflammatory response in primary microglia.
J Surg Res
; 179(1): e219-25, 2013 Jan.
Article
en En
| MEDLINE
| ID: mdl-22683080
ABSTRACT
BACKGROUND:
Neuroinflammation mediated by microglia has been implicated in delirium. Suppression of microglial activation may therefore contribute to alleviate delirium. It has been reported that dexmedetomidine (DEX) has a potent anti-inflammatory property. In the present study, we investigated the effects of DEX on the production of proinflammatory mediators in lipopolysaccharide-stimulated microglia. MATERIALS ANDMETHODS:
The concentrations of DEX were chosen to correspond to 1, 10, and 100 times of clinically relevant concentration (i.e., 1, 10, and 100ng/mL). The levels of proinflammatory mediators, such as inducible nitric oxide synthase or nitric oxide, prostaglandin E(2), interleukin 1ß, and tumor necrosis factor α, were measured.RESULTS:
DEX at 1ng/mL did not affect the production of proinflammatory mediators. DEX at 10 and 100ng/mL significantly inhibited the release of nitric oxide, prostaglandin E(2), interleukin 1ß, and tumor necrosis factor α and the expression of inducible nitric oxide synthase messenger RNA.CONCLUSIONS:
These results suggest that DEX is a potent suppressor of lipopolysaccharide-induced inflammation in activated microglia and may be a potential therapeutic agent for the treatment of intensive care unit delirium.
Texto completo:
1
Bases de datos:
MEDLINE
Asunto principal:
Lipopolisacáridos
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Microglía
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Dexmedetomidina
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Inflamación
/
Antiinflamatorios
Límite:
Animals
Idioma:
En
Revista:
J Surg Res
Año:
2013
Tipo del documento:
Article
País de afiliación:
China