Abstract
Puerarin is a major isoflavone glycoside from the root of Pueraria lobata. It has been reported that puerarin can protect neurons from oxidative stress-induced
apoptosis. Emerging evidence suggests that oxidative damage is associated with Aβ-induced neuronal death. In the current study, we evaluated the effect of puerarin
on Alzheimerʼs disease induced by Aβ and explored the potential mechanisms underlying this effect. We found that the escape
latency of the Morris water maze was decreased in groups treated with puerarin compared
to the model group (p < 0.01). In addition, there were significant differences between
treated groups and the model group mice in a Y-maze test (p < 0.01). Furthermore,
puerarin recovered the levels of brain-derived neurotrophic factor, phosphorylated
tau, malondialdehyde, acetylcholine esterase, glycogen synthase kinase-3beta, and
the activity of superoxide dismutase to some extent in the hippocampus and cerebral
cortex. Shrinkage of nuclei and swollen and eccentrically dispersed neuronal bodies
were observed in the hippocampus of Aβ-treated mice. These data demonstrate that puerarin might protect against cognitive
deficits, oxidative stress, and neurodegeneration induced by Aβ
1–42.
Key words
puerarin -
Pueraria lobata
- Fabaceae - A
β
1–42
- Alzheimerʼs disease - cognitive impairment
