Abstract
Schisandrin is the main active ingredient isolated from Schisandra chinensis Baill. Recent studies have demonstrated that schisandrin exhibits anti-inflammatory effects in vivo and in vitro. In this study, we examined whether the order of lipopolysaccharide (LPS) treatment affects the mechanism of schisandrin anti-inflammatory activity. We found that the antiinflammatory mechanisms are not the same depending on whether macrophages were treated with schisandrin before or after LPS. The main difference is that inhibitor kappaBalpha (IkappaBalpha) degradation was not inhibited when macrophages were pretreated by LPS before schisandrin and was weakly inhibited when macrophages were pretreated by schisandrin before LPS.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Anti-Inflammatory Agents / pharmacology*
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Cell Line
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Cyclooctanes / pharmacology*
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Cyclooxygenase 2 / metabolism
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Dose-Response Relationship, Drug
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I-kappa B Proteins / metabolism
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JNK Mitogen-Activated Protein Kinases / metabolism
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Lignans / pharmacology*
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Lipopolysaccharides / pharmacology*
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Macrophages / drug effects*
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Macrophages / enzymology
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Macrophages / metabolism
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Mice
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NF-KappaB Inhibitor alpha
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NF-kappa B / metabolism
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Nitric Oxide Synthase Type II / metabolism
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Phosphorylation
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Polycyclic Compounds / pharmacology*
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Time Factors
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Transcription Factors / metabolism*
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p38 Mitogen-Activated Protein Kinases / metabolism
Substances
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Anti-Inflammatory Agents
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Cyclooctanes
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I-kappa B Proteins
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Lignans
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Lipopolysaccharides
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NF-kappa B
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Nfkbia protein, mouse
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Polycyclic Compounds
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Transcription Factors
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NF-KappaB Inhibitor alpha
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Nitric Oxide Synthase Type II
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Nos2 protein, mouse
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Ptgs2 protein, mouse
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Cyclooxygenase 2
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JNK Mitogen-Activated Protein Kinases
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p38 Mitogen-Activated Protein Kinases
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schizandrin