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

Authors: Jiao, Jian  Xue, Bing  Zhang, Lei  Gong, Yuntao  Li, Kairong  Wang, Haomin  Jing, Liming  Xie, Junxia  Wang, Xiaomin 
Citation: Jiao J, etal., J Neuroimmunol. 2008 Dec 15;205(1-2):32-6. doi: 10.1016/j.jneuroim.2008.08.006. Epub 2008 Nov 12.
Pubmed: (View Article at PubMed) PMID:19004508
DOI: Full-text: DOI:10.1016/j.jneuroim.2008.08.006

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.


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CRRD Object Information
CRRD ID: 13825252
Created: 2018-12-04
Species: All species
Last Modified: 2018-12-04
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.