Abstract
Triptolide, a biologically active natural product from Tripterygium wilfordii, protects neurons from inflammation-mediated damage. Our results showed for the first time that triptolide inhibited the expression of CXCR2 and presenilin in a neuroblastoma cell line SHSY5Ysw. Moreover, triptolide potently inhibited amyloid-β1-42 production with IC50 value of 30 pM in HEK293sw cells or 2 nM in SHSY5Ysw cells, respectively. We also demonstrated that triptolide prevented primary cortical neurons from chemokine CXCL1-induced cytotoxicity. Therefore, our study indicates that the neural protective effect of triptolide is largely mediated by inhibiting CXCR2 activity.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Amyloid beta-Peptides / antagonists & inhibitors*
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Amyloid beta-Peptides / biosynthesis
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Animals
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Cell Line, Tumor
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Cells, Cultured
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Diterpenes / pharmacology*
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Dose-Response Relationship, Drug
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Epoxy Compounds / pharmacology
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HEK293 Cells
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Humans
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Neurons / drug effects*
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Neurons / metabolism
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Neuroprotective Agents / pharmacology*
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Peptide Fragments / antagonists & inhibitors*
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Peptide Fragments / biosynthesis
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Phenanthrenes / pharmacology*
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Rats
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Receptors, Interleukin-8B / antagonists & inhibitors*
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Receptors, Interleukin-8B / metabolism
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Tripterygium*
Substances
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Amyloid beta-Peptides
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Diterpenes
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Epoxy Compounds
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Neuroprotective Agents
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Peptide Fragments
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Phenanthrenes
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Receptors, Interleukin-8B
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amyloid beta-protein (1-42)
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triptolide