Aim To study the improvement of docosahexaenoic Acid-phosphatidylcholine （DHA-PC） on the cogni- tive deficits of AD rats induced by Aβ25_35, and investigate molecular mechanism of DHA-PC. Methods 1. fifty healthy w...Aim To study the improvement of docosahexaenoic Acid-phosphatidylcholine （DHA-PC） on the cogni- tive deficits of AD rats induced by Aβ25_35, and investigate molecular mechanism of DHA-PC. Methods 1. fifty healthy wistar rats of SPF level, weighing 250 -0 300 g were randomly divided into control group, AD group, done- pezil group, DHA-PC treated group, DHA group. Each group had 10 rats. Aβ25_35 was injected into hippocampus CA1 area of the AD group rats and drug treated group rats. The same volume of Normal saline was injected in the same area of sham group rats, the control group deal with nothing. All the groups were tested with Morris water maze after operation to test whether AD models. Both DHA-PC treated group and DHA treated group were given by oral administration of corresponding drugs. The AD group and sham group were given by oral administration of nor- mal saline, the control group were fed with normal food. All the groups were treated for 30 days. All the groups were tested with Morris water maze on day 25 after administration. We determined the phosphorylated tau protein of Ser396 site with Western Blot and determined the Superoxide dismutase （SOD）. Results The water maze test was performed： The latency period of AD group was increased compared with the sham group （P 〈 0.05）. The DHA- PC group was spent less time to find the platform compared with the AD group （P 〈 0.05）. DHA-PC treated groups used more linear and tendency modes than AD group. In the probe trial, the AD group spent less time in the target area compared with sham group （P 〈0.01 ） , and the DHA-PC group spent more time in the target area compared with AD group （P 〈 0.05 ）. The results of Western blot are as follows ： DHA-PC reduced the phosphoryl- ated tau protein of Ser396 site expression in cortex （P 〈 0.01 ）. The results of SOD in cortex were increased in DHA-PC treated groups than AD groups （P 〈0.01）. Conclusion DHA-PC can improve the cognitive deficits of AD rats, improve the abnormalities and decreased the level of the phosphorylated Ser396 tau protein of AD rats in cortex. DHA-PC can also improve the cognitive deficits of AD rats by increased SOD.展开更多
文摘Aim To study the improvement of docosahexaenoic Acid-phosphatidylcholine （DHA-PC） on the cogni- tive deficits of AD rats induced by Aβ25_35, and investigate molecular mechanism of DHA-PC. Methods 1. fifty healthy wistar rats of SPF level, weighing 250 -0 300 g were randomly divided into control group, AD group, done- pezil group, DHA-PC treated group, DHA group. Each group had 10 rats. Aβ25_35 was injected into hippocampus CA1 area of the AD group rats and drug treated group rats. The same volume of Normal saline was injected in the same area of sham group rats, the control group deal with nothing. All the groups were tested with Morris water maze after operation to test whether AD models. Both DHA-PC treated group and DHA treated group were given by oral administration of corresponding drugs. The AD group and sham group were given by oral administration of nor- mal saline, the control group were fed with normal food. All the groups were treated for 30 days. All the groups were tested with Morris water maze on day 25 after administration. We determined the phosphorylated tau protein of Ser396 site with Western Blot and determined the Superoxide dismutase （SOD）. Results The water maze test was performed： The latency period of AD group was increased compared with the sham group （P 〈 0.05）. The DHA- PC group was spent less time to find the platform compared with the AD group （P 〈 0.05）. DHA-PC treated groups used more linear and tendency modes than AD group. In the probe trial, the AD group spent less time in the target area compared with sham group （P 〈0.01 ） , and the DHA-PC group spent more time in the target area compared with AD group （P 〈 0.05 ）. The results of Western blot are as follows ： DHA-PC reduced the phosphoryl- ated tau protein of Ser396 site expression in cortex （P 〈 0.01 ）. The results of SOD in cortex were increased in DHA-PC treated groups than AD groups （P 〈0.01）. Conclusion DHA-PC can improve the cognitive deficits of AD rats, improve the abnormalities and decreased the level of the phosphorylated Ser396 tau protein of AD rats in cortex. DHA-PC can also improve the cognitive deficits of AD rats by increased SOD.
