Inhibition of iNOS Expression Via Ursodeoxycholic Acid in Murine Microglial Cell, BV-2 Cell Line
Immune Network
;
: 45-49, 2005.
Article
Dans Coréen
| WPRIM
| ID: wpr-127000
ABSTRACT
BACKGROUND:
Inflammation in the brain has known to be associated with the development of a various neurological diseases. The hallmark of neuro-inflammation is the activation of microglia, brain macrophage. Pro-inflammatory compounds including nitric oxide (NO) are the main cause of neuro-degenerative disease such as Alzheimer's disease (AD) which is resulted in cell death. Among those pro-inflammatory compounds, NO contributes to the cell death by directly or indirectly.METHODS:
In the study, we examined whether ursodeoxycholic acid (UDCA), a non-toxic hydrophilic bile acid, inhibits the NO production by a direct method using Griess reagent and by RT-PCR in the gene expression of inducible nitric oxide synthase (iNOS). In signal transduction, we also examined the NF-kappa B (p65/p50), IKK, and Ikappa B, which are associated with the expression of iNOS gene using western blots.RESULTS:
In the present study, we found that UDCA effectively inhibited NO production in BV-2 microglial cell, and NF-kappa B activation was reduced by suppressing IKK gene expression and by increasing the Ikappa B in cytosol comparing those to the positive control LPS.CONCLUSION:
Taken together, these data suggested that UDCA may play a crucial role in inhibiting the NO production and the results imply that UDCA suppresses a cue signal of the microglial activation via stimulators, such as beta-amyloid peptides which are known to stimulate microglia in AD pathogenesis.
Texte intégral:
Disponible
Indice:
WPRIM (Pacifique occidental)
Sujet Principal:
Peptides
/
Acide ursodésoxycholique
/
Bile
/
Encéphale
/
Transduction du signal
/
Expression des gènes
/
Lignée cellulaire
/
Technique de Western
/
Facteur de transcription NF-kappa B
/
Mort cellulaire
langue:
Coréen
Texte intégral:
Immune Network
Année:
2005
Type:
Article
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