The Effects Of Diazoxide On The Change Of Apoptotic Factors And The Ethology Of The Alzheimer's Disease Model Rat

Background The main pathological features is senile plaques,neurofibrillary tangles and degeneration of neurons of Alzheimer disease. The main components of the senile plaques is P-amyloid protein,and Aβ1-42 play an important role. Although the exact pathogeny of AD is unknown, but the widely recognized Aphypothesis considers that A Pstart the process, and plays a key role in its development. Although the specific mechanism is still unclear, but cell toxicity of Aβ, especially apoptosis is always focal point. In vitro studies show that:the energy generation obstacles of mitochondria and lead cell to produce ROS,and lower the activity of the Na+/K+ ATP enzyme in the cell,lead to the apoptosis of cell,all of that is because of Aβ. ATP-sensitive potassium channels is on the cell membranes and mitochondria membranes,and it has several channels. Studies have confirmed that activation of MitoKATP channels could lower the apoptosis of cell. Recent studies show that diazoxide is a MitoKATP opener, it could restrain ischemic and anoxia. We tried to adjusting diazoxide to study its effection in the AD model rat.Objective The investigation is aimed to explore the establishment of AD models of Wistar rat byβ-amyloid1-42 (Aβ1-42) and the effect of diazoxide on the change of apoptotic factors and the ethology of the rat AD models.Methods Aβ1-42 injected into the bilateral ventricles of rats, and two weeks later the AD models were established. Some are injected with diazoxide on the base of the injection of Aβ1-42. We will use Y maze electric stimulation to evalue the capability of study and memory of the rats, and use protein electrophoresis to detect the expression of Bcl-2 and Caspase-3 in cortical layer and hippocampus of the rats.Results Compared with the normal and the ones which injected with NS, the rats which injected with Aβ1-42 made the capability of the study and memory descended,the expression of Bcl-2 decreased and the expression of Caspase-3 increased, P<0.05. Compared with the rats which injected with Aβ1-42,the rats which injected with Aβ1-42 and diazoxide made the capability of the study and memory raised, the expression of Bcl-2 increased and the expression of Caspase-3 decreased, P<0.05.Conclusions The AD models were established by the injection of Aβ1-42 into the bilateral ventricles of rats. Diazoxide can improve the capability of the study and memory, and also can increase the expression of the Bcl-2 and decrease the expression of the Caspase-3. It is likely that diazoxide could resist neurons apoptosis induced by Aβ1-42.