Effect Of Ethology、Enzymology And Apoptosis Of Alzheimer’s Disease Model With Isoliquiritigenin

[Objective] Senile Dementia is the most common illness that seriously affects the health of the old people, currently there is no effective medical treatments. As human society tends to aging, prevention of such disease has become a focal point in medical profession in the world. Isoliquiritigenin, ISL, An effective monomer that is extracted from licorice roots is flavonoids. It is now used as drugs, cosmetics and food additives in medical and food industry. In recent studies it is shown that isoliquiritigenin has anti-tumor, antioxidant, and anti-inflammatory effects. In this experiment we explore the protection effectiveness of isoliquiritigenin to the dementia through the establishment of in vitro and in vivo dementia model. Provide an effective theoretical foundation for the prevention and treatment of Alzheimer’s disease[Methods] This experiment divided two part,in vitro and in vivo.In vivo experiment,the model of dementia mouse were made by intraperitoneal injection of D-gal100mg/kg for50days.The model of dementia mouse given orally20、40mg/kg of ISL protection.Using water maze test and platform experiment and biochemist determining methods to observe the ISL in deficit of learning and memory and MDA level, activities of MAO,TChE in the brain tissue of mouse.In vitro experiment,10μmol/L AP25-35treated NGF-differenciated PC12cell to establish invitro AD medel.The Way of Aβ25-35induced PC12cells injury was analyzed by MTT,LDH method, MDA level and the level of activated Caspase-3detected by Western Blotting.[Rusult] In vivo experiment,the model of dementia mouse body weight were signigicantly decreased.The latent period in platform experiment were statistically shorten and the errors rate were increased (P<0.01). The whole swimming time in water maze test were lengthened and the right through rate were reduced(P<0.05or P<0.01). The activities of MAO and AchE were incresed and contents of MDA from brain tissue were significantly increased in the model group.(P<0.05or P<0.01) which whole changes were antagonized by low, and high dosage of ISL extracts.In vitro experiment,the Aβ25-35injury group cell vibility was statistically decreased in MTT metabolic rate examination.LDH release was increased dramatically. The activated caspase-3protein level and MDA level were dramatically incresed in Aβ25.35injury group (P<0.05or P<0.01), which whole changes were antagonized by low and high dosage of ISL。[Conclusion] The ISL can protect the deficit of learning and memory and the changes in neurobiochemistry on model of dementia mouse. And can protect the cytotoxity and apoptosis of PC12cells induced by Aβ25-35. These data suggest that the ISL can protect the Alzheimer’s Disease.