Triptolide inhibits amyloid-β1-42-induced TNF-α and IL-1β 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 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.