Effects of ginkgolide B on lipopolysaccharide-induced TNFalpha production in mouse peritoneal macrophages and NF-kappaB activation in rat pleural polymorphonuclear leukocytes / 药学学报
Acta Pharmaceutica Sinica
;
(12): 415-418, 2004.
Artigo
em Chinês
| WPRIM
| ID: wpr-302796
ABSTRACT
<p><b>AIM</b>To study the effects of ginkgolide B on lipopolysaccharide (LPS)--induced TNFalpha production in mouse peritoneal macrophages and NF-kappaB activation in rat pleural polymorphonuclear leukocytes.</p><p><b>METHODS</b>L929 crystal violet staining assay was used to show the level of TNFalpha released from mouse peritoneal macrophages induced by LPS. Electrophoretic mobility shift assay (EMSA) was used to determine NF-kappaB binding activities.</p><p><b>RESULTS</b>Ginkgolide B (1, 10 micromol x L(-1)) was shown to significantly inhibit LPS (10 mg x L(-1))-induced TNFalpha production in mouse peritoneal macrophages, the IC50 was 0.26 micromol x L(-1); LPS (1 mg x L(-1)) and PAF (1 nmol , L(-1)) were shown to increase the NF-kappaB binding activities in rat pleural polymorphonuclear leukocytes; ginkgolide B (10 micromol x L(-1)) was found to inhibit LPS (1 mg x L(-1))-induced NF-kappaB activation in rat pleural polymorphonuclear leukocytes; ginkgolide B (1, 10 micromol x L(-1)) was shown to inhibit PAF (1 nmol x L(-1))-induced NF-kappaB activation in rat pleural polymorphonuclear leukocytes.</p><p><b>CONCLUSION</b>The inhibition of NF-kappaB activation and TNFalpha production might be considered to be part of the mechanisms underlying the antiinflammatory action of ginkgolide B; PAF is involved in activation of the NF-kappaB pathway stimulated with LPS.</p>
Texto completo:
DisponíveL
Índice:
WPRIM (Pacífico Ocidental)
Assunto principal:
Farmacologia
/
Plantas Medicinais
/
Fator de Ativação de Plaquetas
/
Química
/
Anti-Inflamatórios não Esteroides
/
Lipopolissacarídeos
/
NF-kappa B
/
Fator de Necrose Tumoral alfa
/
Ratos Wistar
/
Macrófagos Peritoneais
Limite:
Animais
Idioma:
Chinês
Revista:
Acta Pharmaceutica Sinica
Ano de publicação:
2004
Tipo de documento:
Artigo
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