Antioxidation Effects And Mechanism Of Flavonoid In AD Rat Models

Objective:To explore the anti-oxidation molecule mechanism of Acer truncatum Bunge Flavonoid from the behavioral and molecular level and provide the experimental foundations for clinical treatment of AD, the Aβ1-42 and D-galactose AD rat model was established.Methods:Thirty-six rats were divided into three groups at random:sham group, model group and treatment group. Aging rats model were established by lateral ventricle injection of Aβ1-42 and abdominal cavity injection of D-Galactose to the rats. Meantime, rats were treated by intragastric administration Acer truncatum Bunge Flavonoid. Then experimental rats were examined spatial memory with the Morris water maze (MWM). Malondialdehyde (MDA),and antioxidants including glutathione (GSH), glutathione reductase (GR), glutathione peroxidase (GSH-Px), superoxide dismutase (SOD) activities were examined by colorimetric method in cerebral cortex. The concentration of the extracellular signal-regulated kinase(ERK), p38 and c-Jun N-terminal kinases(JNK), P-ERK, P-P38, P-JNK were examined by western blotting methods.Results:The AD model rats when compared with control group exhibited a significant increase in escape latencies (P<0.05), while a decrease in the time of staying at the first quadrants of platform and the degree of crossing over a platform. The cerebral cortex concentration of the MDA was increased, and the concentration of the GR, GSH-PX were decreased (P<0.05). The expression of P-p38, P-JNK were increased while P-ERK was decreased (P<0.05). After the treatment of the he Flavonoid from the Leaves of Acer truncatum Bunge, the AD model rats exhibited a significant decrease in escape latencies (P<0.05), an obvious increase in the time of staying the first quadrants of platform (P<0.05)and the increase of crossing over a platform(P<0.05) when compared with the AD group(P<0.05). The concentration of the MDA was decreased, the concentration of GR, GSH-PX were increased (P<0.05). The expression of the P-p38, P-JNK were less than the AD model while P-ERK was more than the AD model (P<0.05). But there were no significant differences between the three groups in the expression of theP38, JNK, ERK (P>0.05).Conclusions:(1) Aβ1-42 combinated with D-galactose could impair the oriented learning and memory capacity and induce the neurodegeneration of central nervous systems in model rats by oxidative stress wich results in P38, JNK phosphorylation increased and ERK phosphorylation inhibition. (2) Acer truncatum Bunge Flavonoid could improve the oriented learning and memory capacity and prevent the neurodegeneration of central nervous systems in aging model rats by antioxidants increased wich induce P38, JNK phosphorylation inhibition and ERK phosphorylation increased.