Objective: To observe the effect of GETO on expression of PSD-95 and Shank-1 protein in postsynaptic dense zone in Alzheimer disease (AD) model rats.
Methods: The AD model rats were established by beta-amyloid protein (Abeta(1-42)) injection into hippocampus CA1 zone. They were assigned into the model group, the donepezil treated group and the GETO treated group, besides, a normal group was set for control. Four weeks after modeling, Morris water maze test was applied to determine the learning and memory function of the AD rats, the number of PSD-95 and Shank-1 protein positive neuron as well as the optical density (OD) in post-synaptic dense zone of hippocampus CA1 area were determined by using immuno-histochemical stain and computerized graphic analysis techniques.
Results: Morris water maze test showed that the mean escape latent period (MELP) of the model rats obviously prolonged than that of the normal rats, and the times of traversing flat roof obviously decreased (P < 0.01), while in the model rats after being treated by GETO, the two parameters were significantly shortened and increased respectively (P < 0.01), reaching the level insignificantly different to those in the donepezil group and the normal group. Immunohistochemical test showed that the number of positive stained neuron of PSD-95 and Shank-1 in hippocampus CA1 zone in the model group was significantly different to those in the normal group (P < 0.01), while in the GETO group those indexes were insignificantly different to those in the donepezil group and the normal group (P > 0.05), but showed a significant difference when compared with those in the model group (P < 0.05).
Conclusion: GETO can obviously improve the function of learning and memory of AD rats induced by Abeta(1-42), and the mechanism may be associated with its actions in improving expressions of PSD-95 and Shank-1 protein in hippocampus CA1 zone, and recovering the structure and function of synapse and enhancing its plasticity.