Abstract: OBJECTIVE: To examine the effects of Cuzhi liquid on learning and memory abilities in a mouse model of Alzheimer's disease(AD).METHODS: One hundred mice were divided into the normal, AD model, piracetam group, Cuzhi liquid low dose and Cuzhi liquid high dose, each group 20 mice. The AD mouse model was induced by daily intraperitoneal injection of D-galactose and sodium nitrite. AD mice then received intragastric administration of piracetam or Cuzhi liquid for60 d, and changes in learning and memory abilities were assessed using the water maze test. The activity of acetylcholinsterase(AchE) and monamine oxidase(MAO), and the levels of nitrogen monoxidum(NO) and malonaldehyde(MDA), were measured in brain tissues. Amyloid protein deposition was assessed by methyl violet staining, and B-cell lymphoma-2(Bcl-2) expression in the hippocampal cornus ammonis 1 region was detected by immunohistochemistry.RESULTS: In the water maze test, the escape latency of the model group was longer than that of the normal group(P < 0.01). The escape latency of the three using drug treatment groups was significantly less than that of the normal group(P < 0.05). The activity of AchE and MAO, and the levels of NO and MDA, in the brain of the model group were significantly higher than that of the normal group(P < 0.05). AchE activity showed a greater reduction in the two Cuzhi liquid groups compared with the piracetam group(P < 0.01), to levels similar to the normal group. There were no differences in MAO activity or NO levels between the three drug treatment groups, while MDA levels were reduced more in the high-dose Cuzhi liquid group compared with the other treatment groups(P < 0.01). Hippocampal Bcl-2 expression was significantly reduced in the model group compared with the normal group(P < 0.01), but significantly improved in the three drug treatment groups(P < 0.05). The high-dose Cuzhi liquid group showed a significantly greater recovery in Bcl-2 expression compared with the other treatment groups.CONCLUSION: Cuzhi liquid can improve learning and memory impairment in an AD mouse model.The mechanism of action may relate to reduced AchE and MAO activity, and reduced NO and MDA levels, in the brain, and improved Bcl-2 expression,an inhibitor of apoptosis.

Key words: Alzheimer disease, Learning, Memory, Acetylcholinesterase, Oxidoreductases, Nitric ox ide, Malondialdehyde, Amyloidogenic proteins, Lymphoma,B-cell, Cuzhi liquid