Inhibition of iNOS Expression Via Ursodeoxycholic Acid in Murine Microglial Cell, BV-2 Cell Line

Seong-Soo Joo, Tae-Joon Won, Kwang-Woo Hwang, Do-Ik Lee

Research output: Contribution to journalArticlepeer-review


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.

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-κB (p65/p50), IKK, and IκB, which are associated with the expression of iNOS gene using western blots.

In the present study, we found that UDCA effectively inhibited NO production in BV-2 microglial cell, and NF-κB activation was reduced by suppressing IKK gene expression and by increasing the IκB in cytosol comparing those to the positive control LPS.

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 asβ-amyloid peptides which are known to stimulate microglia in AD pathogenesis.
Original languageEnglish (US)
Pages (from-to)45-49
JournalImmune Network
Issue number1
StatePublished - 2005
Externally publishedYes


  • Nitric oxide
  • Alzheimer's disease
  • ursodeoxycholic acid
  • NF-κB
  • iNOS


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