From The Perspective Of Glucose Metabolism To Discuss The Mechanism Of Prevention And Treatment Effect Of Abnormal Savda Munziq On Alzheimer Disease Rat Model With Abnormal Savda Syndrome

Objective From the Perspective of Glucose Metabolism to reveal abnormal savda munziq AD prevention mechanisim and Provide experimental evidence for the clinical application of abnormal Savda Munziq treat AD.Methods Methodes:Establish abnormal Savda syndrome rat model using classical method, then injected (3-Amyloid 1-40 (βAmyloid 1-40, Aβ1-40,)on hippocampus to establish the Alzheimer’s disease carrying abnormal Savda syndrome rat model,96 SD rats were randomly divided into 7 groups that,black control group, Abnormal Savda syndrome group, Alzheimer’s rat model with Abnormal Savda syndrome group, Alzheimer’s rat model group, ASMq group (low dose, middle dose and high dose) and positive control (Donepezil)group.Testing the behavioral changes with Morris water maze test, separate the hippocampus and by using HPLC method to detect the rat hippocampus ATP, ADP and AMP content, observing the biological characterization after the Na+ - K+-ATPase、Ca 2+- Mg 2+-ATPase、SDH test.Using immunohistochemical method to observe the glucose transporters 1.2.3.4 and the expression of insulin receptor.Results HPLC results show that compared with the black control group, in Abnormal Savda syndrome group, Alzheimer’s rat model with Abnormal Savda syndrome group, Alzheimer’s rat model group, the level of ATP, ADP and AMP has significantly decreased. (P<0.05); compared with Alzheimer’s rat model with Abnormal Savda syndrome group the level of ATP, ADP and AMP has significantly increased in ASMq group(P<0.05); compared with positive control (Donepezil)group. in ASMq group the level of ATP, ADP and AMP was significantly increased (P<0.05); Morris water maze test show that compared with the black control group, in Abnormal Savda syndrome group, Alzheimer’s rat model with Abnormal Savda syndrome group, Alzheimer’s rat model group, escape latency extend obviously,The difference was statistically significant (P<0.05); compared with Alzheimer’s rat model group, Alzheimer’s rat model with Abnormal Savda syndrome group, in ASMq group escape latency to be markedly reduced,The difference was statistically significant (P<0.01); compared with Alzheimer’s rat model group, Alzheimer’s rat model with Abnormal Savda syndrome group escape latency obviously extended,the difference was statistically significant (P<0.01) Mitochondrial enzyme activity Test results show that compared with the black control group, in Abnormal Savda syndrome group, Alzheimer’s rat model with Abnormal Savda syndrome group, Alzheimer’s rat model group, Na+-K+-ATPase and Ca2+-Mg2+-ATPasee, SDH Activity significantly reduced. (P<0.05); compared with Alzheimer’s rat model group, Alzheimer’s rat model with Abnormal Savda syndrome group Na+-K+-ATPase and Ca2+-Mg2+-ATPasee, SDH Activity significantly reduced. (P<0.05); compared with Alzheimer’s rat model group, Alzheimer’s rat model with Abnormal Savda syndrome group, in ASMq group Na+-K+-ATPase and Ca2+-Mg2+-ATPasee, SDH Activity significantly increased (P<0.05); compared with Alzheimer’s rat model group, Alzheimer’s rat model with Abnormal Savda syndrome group, Na+-K+-ATPase and Ca2+-Mg2+-ATPasee, SDH Activity significantly reduced. (P<0.05); compared with Alzheimer’s rat model group,compared with positive control (Donepezil)group. in ASMq group the level of ATP, ADP and AMP was significantly increased (P<0.05); compared with the black control group, in Abnormal Savda syndrome group, Alzheimer’s rat model with Abnormal Savda syndrome group, Alzheimer’s rat model group, Mitochondrial protein content was significantly reduced, he difference was statistically significant (P<0.05); compared with Alzheimer’s rat model group, Alzheimer’s rat model with Abnormal Savda syndrome group Mitochondrial protein content was significantly reduced, the difference was statistically significant (P<0.05); compared with Alzheimer’s rat model group, Alzheimer’s rat model with Abnormal Savda syndrome group, in ASMq group Mitochondrial protein content was significantly increased, the difference was statistically significant (P<0.05); Immunohistochemical results show that in Abnormal Savda syndrome group, Alzheimer’s rat model with Abnormal Savda syndrome group, Alzheimer’s rat model group, glucose transporters1.2.3.4 and the expression of insulin receptor significantly reduced, the difference was statistically significant (P<0.05); compared with Alzheimer’s rat model group, Alzheimer’s rat model with Abnormal Savda syndrome group, glucose transporters 1.2.3.4 and the expression of insulin receptor significantly reduced, the difference was statistically significant (P<0.05); compared with Alzheimer’s rat model group, Alzheimer’s rat model with Abnormal Savda syndrome group, in ASMq group glucose transporters1.2.3.4 and the expression of insulin receptor significantly increased, the difference was statistically significant (P<0.05); Conclusion aabnormal savda munziq has obvious improvement and therapeutic role that disturbance of energy metabolism on Alzheimer’s rat model with abnormal savda syndrome brain tissue.