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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Published in | Acta pharmacologica Sinica Vol. 29; no. 2; pp. 245 - 251 |
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Main Authors | , , , , |
Format | Journal Article |
Language | English |
Published |
London
Nature Publishing Group UK
01.02.2008
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Subjects | |
Online Access | Get full text |
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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. |
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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 |