Central interleukin-10 attenuated lipopolysaccharide-induced changes in core temperature and hypothalamic glutamate, hydroxyl radicals and prostaglandin-E(2).
Eur J Pharmacol
; 654(2): 187-93, 2011 Mar 05.
Article
em En
| MEDLINE
| ID: mdl-21237148
ABSTRACT
It has been documented that intravenous lipopolysaccharide (LPS) in rabbits causes fever accompanied by increased levels of extracellular glutamate, hydroxyl radicals, and prostaglandin E(2) (PGE(2)) in the hypothalamus and circulating tumor necrosis factor-alpha (TNF-α). This investigation was to determine whether central interleukin-10 (IL-10) exerted its antipyresis by reducing changes in circulating TNF-α and extracellular glutamate, hydroxyl radicals and PGE(2) in the hypothalamus. The microdialysis probes were stereotaxically and chronically implanted into the preoptic anterior hypothalamus of rabbit brain for determinating extracellular glutamate, hydroxyl radicals, and PGE(2) in situ. It was found that systemically injected LPS (2µg/kg, intravenously) increased the levels of core temperature, and extracellular glutamate, hydroxyl radicals, and PGE(2) in the hypothalamus accompanied by increased plasma levels of TNF-α. Pretreatment with IL-10 (10-100ng, intracerebroventricularly) 1h before intravenous LPS significantly reduced the LPS-induced changes in extracellular glutamate, hydroxyl radicals, and PGE(2) in the hypothalamus and fever, but not the increased levels of TNF-α in rabbits. These findings suggested that directly injected IL-10 into the lateral cerebral ventricle 1h before intravenous LPS exerted its antipyresis by inhibiting the changes in extracellular glutamate, hydroxyl radicals and PGE(2) in the hypothalamus during LPS fever in rabbits.
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Temperatura Corporal
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Dinoprostona
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Lipopolissacarídeos
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Fator de Necrose Tumoral alfa
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Interleucina-10
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Radical Hidroxila
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Ácido Glutâmico
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Hipotálamo
Limite:
Animals
Idioma:
En
Revista:
Eur J Pharmacol
Ano de publicação:
2011
Tipo de documento:
Article