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Effects of Cistanche Polysaccharide on Learning and Cholinergic System of Brain Tissue in Alzheimer's Disease Rats

Author(s): G. Yin*, Xiaohui Hu, S. Xie and Daokai Gong
Department of Neurology, Jingzhou Hospital Affiliated to Changjiang University, Jingzhou, Hubei 434002, China

Correspondence Address:
G. Yin, Department of Neurology, Jingzhou Hospital Affiliated to Changjiang University, Jingzhou, Hubei 434002, China, E-mail:

To investigate the effect of Cistanche deserticola polysacchrides on learning and memory ability, and cholinergic system in rats; replicate Alzheimer's disease rat model using amyloid beta1-40 lateral ventricular injection, randomly divided into sham group, model group, low, medium and high polysaccharide dose (50, 100, 200 mg/kg) group. For 28 d, the effect of Cistanche polysaccharide on learning and memory in rats was measured by Morris water maze and escape latency was calculated. Escape latency significantly decreased compared with preoperative (p<0.01), after lateral ventricular injection in each group significantly decreased compared with normal and sham group (p<0.01). The incubation period of rats in the administration group decreased significantly compared with 7 d, but the Cistanche deserticola group was significantly increased compared with normal and sham group (p<0.01). Compared with the sham group, acetylcholinesterase vitality was significantly increased and acetylcholine transferase vitality was significantly decreased in the model group (p<0.05), indicating that amyloid beta1-40 impaired acetylcholinesterase and acetylcholine transferase in rat cortex and hippocampus. Cistanche deserticola polysaccharides significantly increased acetylcholine transferase activity (p<0.05). Acetylcholinesterase viability was significantly suppressed in the Cistanche deserticola polysaccharides high-dose group. The learning and memory ability of Alzheimer disease rats is improved, and the mechanism is related to the effect on the cholinergic system. Cistanche deserticola polysaccharides not only enhances acetylcholine transferase activity but also decreases acetylcholinesterase activity, showing that it may inhibit amyloid beta1-40 by increasing acetylcholine activity in the brain leading to learning and memory dysfunction in rats. 

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