Tetrandrine suppresses lipopolysaccharide-induced microglial activation by inhibiting NF-[kappa]B pathway

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. The microglia pretreated with or without TET were acti...

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Published inActa pharmacologica Sinica Vol. 29; no. 2; p. 245
Main Authors Xue, Yang, Wang, Ying, Feng, De-chun, Xiao, Bao-guo, Xu, Ling-yun
Format Journal Article
LanguageEnglish
Published Shanghai Nature Publishing Group 01.02.2008
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Abstract 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. 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-alpha and interleukin-6 (IL-6) production by microglia were measured afterwards. Electrophoretic mobility shift assay was performed to determine whether NF-kappaB activity in microglia was affected by TET treatment. 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-alphaand IL-6 in LPS-induced microglial activation. Such suppressive effect was accompanied by inhibiting transcription factor NF-kappaB activation. Our results suggest that TET might modulate LPS-induced microglial activation by inhibiting the NF-kappaB-mediated release of inflammatory factors.
AbstractList 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. 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-alpha and interleukin-6 (IL-6) production by microglia were measured afterwards. Electrophoretic mobility shift assay was performed to determine whether NF-kappaB activity in microglia was affected by TET treatment. 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-alphaand IL-6 in LPS-induced microglial activation. Such suppressive effect was accompanied by inhibiting transcription factor NF-kappaB activation. Our results suggest that TET might modulate LPS-induced microglial activation by inhibiting the NF-kappaB-mediated release of inflammatory factors.
Author Xiao, Bao-guo
Feng, De-chun
Wang, Ying
Xue, Yang
Xu, Ling-yun
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