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.
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Authors | Ju Wang, Zi-Qi Shi, Xiaojun Xu, Gui-Zhong Xin, Jun Chen, Lian-Wen Qi, Ping Li |
Journal | Journal of Alzheimer's disease : JAD
(J Alzheimers Dis)
Vol. 33
Issue 1
Pg. 217-29
( 2013)
ISSN: 1875-8908 [Electronic] Netherlands |
PMID | 22986777
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Amyloid beta-Peptides
- Diterpenes
- Epoxy Compounds
- Neuroprotective Agents
- Peptide Fragments
- Phenanthrenes
- Receptors, Interleukin-8B
- amyloid beta-protein (1-42)
- triptolide
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Topics |
- Amyloid beta-Peptides
(antagonists & inhibitors, biosynthesis)
- Animals
- Cell Line, Tumor
- Cells, Cultured
- Diterpenes
(pharmacology)
- Dose-Response Relationship, Drug
- Epoxy Compounds
(pharmacology)
- HEK293 Cells
- Humans
- Neurons
(drug effects, metabolism)
- Neuroprotective Agents
(pharmacology)
- Peptide Fragments
(antagonists & inhibitors, biosynthesis)
- Phenanthrenes
(pharmacology)
- Rats
- Receptors, Interleukin-8B
(antagonists & inhibitors, metabolism)
- Tripterygium
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