Triptolide inhibits amyloid-beta1-42-induced TNF-alpha and IL-1beta production in cultured rat microglia

Microglia plays an important role in mediating neuroinflammation in Alzheimer's disease (AD). Intervention in microglia activation may exert a neuroprotective effect. In the present study, we reported that oligomeric Abeta1-42 dramatically increased the level of tumor necrosis factor (TNF)-alph...

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Bibliographic Details
Published in:Journal of neuroimmunology 2008-12, Vol.205 (1-2), p.32-36
Main Authors: Jiao, Jian, Xue, Bing, Zhang, Lei, Gong, Yuntao, Li, Kairong, Wang, Haomin, Jing, Liming, Xie, Junxia, Wang, Xiaomin
Format: Article
Language:English
Subjects:
Amyloid beta-Peptides - pharmacology
Analysis of Variance
Animals
Animals, Newborn
Brain - cytology
Cells, Cultured
Diterpenes - pharmacology
Dose-Response Relationship, Drug
Enzyme-Linked Immunosorbent Assay - methods
Epoxy Compounds - pharmacology
Immunosuppressive Agents - pharmacology
Interleukin-1beta - metabolism
Microglia - drug effects
Peptide Fragments - pharmacology
Phenanthrenes - pharmacology
Rats
Rats, Sprague-Dawley
Time Factors
Tumor Necrosis Factor-alpha - metabolism
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Summary:Microglia plays an important role in mediating neuroinflammation in Alzheimer's disease (AD). Intervention in microglia activation may exert a neuroprotective effect. In the present study, we reported that oligomeric Abeta1-42 dramatically increased the level of tumor necrosis factor (TNF)-alpha and interleukin (IL)-1beta compared to monomeric and fibrillar Abeta1-42 in rat microglial cultures. Pretreatment of the cultures with triptolide, an anti-inflammatory reagent, alleviated the elevation of TNF-alpha and IL-1beta level induced by oligomeric Abeta1-42. Our results showed that oligomeric Abeta played an important role in mediating neuroinflammation and triptolide was able to suppress the production of pro-inflammatory cytokines from microglia.
ISSN:0165-5728
1872-8421
DOI:10.1016/j.jneuroim.2008.08.006