Abstract
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 Aβ1-42 dramatically increased the level of tumor necrosis factor (TNF)-α and interleukin (IL)-1β compared to monomeric and fibrillar Aβ1-42 in rat microglial cultures. Pretreatment of the cultures with triptolide, an anti-inflammatory reagent, alleviated the elevation of TNF-α and IL-1β level induced by oligomeric Aβ1-42. Our results showed that oligomeric Aβ played an important role in mediating neuroinflammation and triptolide was able to suppress the production of pro-inflammatory cytokines from microglia.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
