This study was performed to determine if
acetylpuerarin (compound N-2211) could reduce amyloid-beta1-42 (Abeta1-42) 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 (Abeta1-42 injected), low-dose and high-dose
acetylpuerarin groups. The
acetylpuerarin groups received peritoneal
acetylpuerarin every day for 12 days after 2 weeks of Abeta1-42 (5 microg/1 microl) 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 (Ibal),
protein kinase C delta (PKCdelta),
IkappaB kinase beta (IKKbeta), and
inducible nitric oxide synthase (iNOS) in hippocampus. After Abeta1-42 injection, the learning and memory abilities of rats were reduced, and
acetylpuerarin treatment ameliorated the observed deficits. Abeta1-42 injection resulted in microglia transforming from resting microglia into an activated state, but this was reduced by
acetylpuerarin treatment. Furthermore, hippocampal expression of PKCdelta, IKKbeta, and iNOS increased following Abeta1-42 treatment, and
acetylpuerarin could suppressed the levels of PKCdelta, iNOS, and IKKbeta.
Acetylpuerarin improves learning and memory functions in Abeta1-42 induced rat models. These effects may be due to anti-neuroinflammatory effects.