Background: Abnormal amyloid β (Aβ) accumulation and deposition in the hippocampus is
an essential process in Alzheimer’s disease (AD).
Objective: To investigate whether Oleanolic acid (OA) could improve memory deficit in AD model
and its possible mechanism.
Methods: Forty-five SD rats were randomly divided into sham operation group, model group, and OA
group. AD models by injection of Aβ25-35 were built. Morris water maze (MWM) was applied to investigate
learning and memory, transmission electron microscope (TEM) to observe the ultrastructure of
synapse, western blot to the proteins, electrophysiology for long-term potentiation (LTP), and Ca2+
concentration in synapse was also measured.
Results: The latency time in model group was significantly longer than that in sham operation group
(P=0.0001); while it was significantly shorter in the OA group than that in model group (P=0.0001);
compared with model group, the times of cross-platform in OA group significantly increased
(P=0.0001). TEM results showed OA could alleviate neuron damage and synapses changes induced by
Aβ25-35. The expressions of CaMKII, PKC, NMDAR2B, BDNF, TrkB, and CREB protein were significantly
improved by OA (P=0.0001, 0.036, 0.041, 0.0001, 0.0001, 0.026, respectively) compared
with that in model group; the concentration of Ca2+ was significantly lower in OA group (1.11±0.42)
than that in model group (1.68±0.18); and the slope rate (P=0.0001) and amplitude (P=0.0001) of f-
EPSP significantly increased in OA group.
Conclusion: The present results support that OA could ameliorate Aβ-induced memory loss of AD
rats by maintaining synaptic plasticity of the hippocampus.