Abstract

Objective To investigate the treatment effect ofcurcumin on Alzheimer's disease in mice and its related mechanism to provide a theoretical reference for the treatment of AD.Methods Forty-eight Kunming mice with APP/PSI transgenosis were randomly divided into four groups:AD model group,AD model+low-dose curcumin group,AD model+middle-dose curcumin group,AD model+high-dose curcumin group (n=12); mice in these later three groups were intraperitoneally injected curcumin at the dosages of 100 mg/(kg ·d),200 mg/(kg·d) and 400 mg/(kg ·d),respectively (once diary for a consecutive 14 d).Another 12 healthy mice were selected as normal control group.Traction test and Morris water maze test were used to observe the behavioral changes of mice in each group;immunohistochemical staining was used to detect the Shank1 and PSD95 expressions in brain tissues of mice in each group; and Western blotting was used to detect the Shank1 and PSD95 protein expression.Results There were significant differences between normal control group and both AD model group and AD model+low-dose curcumin group in average scores,escape latency and frequency through the original platform and dwell time percentages in the original platform quadrant in the traction experiments,positive cell counts and average gray scale of Shank1 and PSD95 (P<0.05).Significant differences were noted between AD model+middle-dose curcumin group and AD model group in average scores,escape latency and frequency through the original platform,dwell time percentages in the original platform quadrant in traction experiments,positive cell counts and average gray scale of Shank1 and PSD95 (P<0.05).As compared with AD model group,the AD model+low-dose curcumin group,AD model+middle-dose curcumin group and AD model+high-dose curcumin group showed significantly different Shank1 and PSD95 protein expressions (P<0.05).Conclusion The middle-dose curcumin application can better improve athletic ability,learning ability and memory capacity of the AD model mice,whose mechanism may be the improvement of shank1 and PSD9 related synaptic and synaptic structure to increase the number of synapses in hippocampus of AD model mice,thereby improving synaptic plasticity. Key words: Curcumin; Alzheimer's disease; Shank1; PSD95

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