Artemisinin Attenuates Amyloid-Induced Brain Inflammation and Memory Impairments by Modulating TLR4/NF-κB Signaling

The abnormal immune response is an early change in the pathogenesis of Alzheimer's disease (AD). Microglial activation is a crucial regulator of the immune response, which contributes to progressive neuronal injury by releasing neurotoxic products. Therefore, finding effective drugs to regulate microglial homeostasis and neuroinflammation has become a new AD treatment strategy. Artemisinin has potent anti-inflammatory and immune activities. However, it is unclear whether Artemisinin contributes to the regulation of microglial activation, thereby improving AD pathology. This study found that Artemisinin significantly reduced amyloid beta-peptide 1-42 (A beta(1-42))-induced increases in nitric oxide and reactive oxygen species and inflammatory factors in BV2 cells. In addition, Artemisinin inhibited the migration of microglia and prevented the expansion of the inflammatory cascade. The mechanical studies showed Artemisinin inhibited neuroinflammation and exerted neuroprotective effects by regulating the Toll-like receptor 4 (TLR4)/Nuclear factor-kappa B (NF-kappa B) signaling pathway. Similar results were obtained in AD model mice, in which Artemisinin administration attenuated A beta(1-42)-induced neuroinflammation and neuronal injury, reversing spatial learning and memory deficits. The anti-inflammatory effect of Artemisinin is also accompanied by the activation of the TLR4/NF-kappa B signaling pathway in the animal model. Our results indicate that Artemisinin attenuated A beta(1-42)-induced neuroinflammation and neuronal injury by stimulating the TLR4/NF-kappa B signaling pathway. These findings suggest that Artemisinin is a potential therapeutic agent for AD.

Automated summary

The abnormal immune response in Alzheimer's disease can be improved by regulating microglial activation and neuroinflammation using Artemisinin.