Tansform Of The Apoptosis-Related Rpoteins In The Multi-Infarct Dementia Rats' CPU And The Effects Of Ginsenogside Rg₂ On It

Objective To observe the transform of the apoptosis-related proteins in themulti-infarct dementia rats' CPU and to investigate the mechanism of the malfunction of its learning and memory. To study the effects of ginsenoside Rg2 on it and to investigate the effects and the possible pharmacological mechanisms of the drug.Methods To inject the thromboinducer compounds into the left hemisphereform the left common carotid artery and the internal carotid artery of the rats to induce the formation of the thrombus in the left hemisphere to establish a rat model with malfunction of learning and memory . Different dosages of ginsenoside Rg2 were given respectively for treatment for 7 days (contrasting with nimodipine) . Measure their abilities of learning and memory with their performance in the Y-maze; observe the pathological changes of their cerebral histology in the NISSLE staining brain sections and measure the expressions of Glu,Calpain II, Caspase - 3 , Bax with immunohistochemistry method.Results The injecting of thrombroinducer compounds defected the abilities oflearning and memory of the MID model rats in the Y-maze ,which is obviously different compared with the sham group (P < 0.05) .In NISSLE staining brain sections of the rats, mini-infarcting spots which has been organized by the glial cells can be found in CPU district. Compared with the model group in the immunohistochemistry results, the expressions of Glu Calpain II , Caspase -3 , Bax are lower in the Rg2 groups and the nimodipine group.Conclusion Injecting thrombroinducer compounds into oneside hemisphere can defect the learning and memory abilites of the rats , which could partly model thebehavior and pathological characterization of multi-infarct dementia . Ginsenoside Rg2 can improve the learning and memory performances of multi-infarct dementia model rats obviously . It maybe the mechanism of ginsenoside Rg2 's protecting effect that decreases the expression of pro - apoptotic proteins such as Calpainll , Caspase -3, Bax...