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Tetrandrine suppresses lipopolysaccharide‐induced microglial activation by inhibiting NF‐κB pathway 1
Author(s) -
XUE Yang,
WANG Ying,
FENG Dechun,
XIAO Baoguo,
XU Lingyun
Publication year - 2008
Publication title -
acta pharmacologica sinica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.514
H-Index - 90
eISSN - 1745-7254
pISSN - 1671-4083
DOI - 10.1111/j.1745-7254.2008.00734.x
Subject(s) - tetrandrine , lipopolysaccharide , nf κb , microglia , chemistry , nfkb1 , pharmacology , microbiology and biotechnology , signal transduction , medicine , inflammation , biology , immunology , biochemistry , gene , transcription factor
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 (O 2 ‐ ) 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 O 2 ‐ , 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.

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