Acetylpuerarin reduces inflammation and improves memory function in a rat model of Alzheimer's disease induced by Aβ1-42

This study was performed to determine if acetylpuerarin (compound N-2211) could reduce amyloid-β1-42(Aβ1-42) induced learning and memory deficits and to examine its anti-neuroinflammatory effects in a rat model. Forty Wistar rats were randomly divided into four groups (n = 10 each): control, model (Aβ1-42 injected), low-dose and high-dose acetylpuerarin groups. The acetylpuerarin groups received peritoneal acetylpuerarin every day for 12 days after 2 weeks of Aβ1-42 (5 μg/1 μl) intrahippocampal injections. The Morris water maze (MWM) was used to assess rats' learning and memory abilities. Immunohistochemistry was used to assess expression levels of ionized calcium-binding adaptor molecule (Iba1), protein kinase C delta (PKCδ), IκB kinase β (IKKβ), and inducible nitric oxide synthase (iNOS) in hippocampus. After Aβ1-42 injection, the learning and memory abilities of rats were reduced, and acetylpuerarin treatment ameliorated the observed deficits. Aβ1-42 injection resulted in microglia transforming from resting microglia into an activated state, but this was reduced by acetylpuerarin treatment. Furthermore, hippocampal expression of PKCδ, IKKβ, and iNOS increased following Aβ1-42 treatment, and acetylpuerarin could suppressed the levels of PKCδ, iNOS, and IKKβ. Acetylpuerarin improves learning and memory functions in Aβ1-42 induced rat models. These effects may be due to anti-neuroinflammatory effects.