Tetrandrine suppresses lipopolysaccharide-induced microglial activation by inhibiting NF-κB pathway

Aim: Microglial activation has been implicated in many neurological diseases. In this study, we examined the effects of tetrandrine (TET), a major pharmacologically-active compound of Chinese herb Stephania tetrandra S Moore on microglial activation. Methods: The microglia pretreated with or without...

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Bibliographic Details
Published inActa pharmacologica Sinica Vol. 29; no. 2; pp. 245 - 251
Main Authors Xue, Yang, Wang, Ying, Feng, De-chun, Xiao, Bao-guo, Xu, Ling-yun
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 01.02.2008
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Summary:Aim: Microglial activation has been implicated in many neurological diseases. In this study, we examined the effects of tetrandrine (TET), a major pharmacologically-active compound of Chinese herb Stephania tetrandra S Moore on microglial activation. Methods: The microglia pretreated with or without TET were activated by lipopolysaccharide (LPS) in vitro. Nitric oxide (NO) release, superoxide anion (O2^-) generation, as well as TNF-α and interleukin-6 (IL-6) production by microglia were measured afterwards. Electrophoretic mobility shift assay was performed to determine whether NF-κB activity in microglia was affected by TET treatment. Results: We found that TET inhibited the LPS-induced activation of microglia by decreasing the production of NO and O2^-, consequently affecting the release of TNF-α and IL-6 in LPS-induced microglial activation. Such suppressive effect was accompanied by inhibiting transcription factor NF-κB activation. Conclusion: Our results suggest that TET might modulate LPS-induced microglial activation by inhibiting the NF-κB-mediated release of inflammatory factors.
Bibliography:cytokine
NF-κB
nitric oxide
tetrandrine; microglia; nitric oxide; superoxideanion; cytokine; NF-κB
R741
superoxideanion
tetrandrine
microglia
31-1347/R
ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:1671-4083
1745-7254
DOI:10.1111/j.1745-7254.2008.00734.x