Zuogui Pill on Heat Shock Protein 70 and Ultrastructure of Brain Neurons in Senile Dementia Model Rats

Alzheimer's disease is a pathological mechanism of chronic degenerative disease of brain function, which has a profound influence on various brain diseases, with the highest incidence in the elderly population. With the deepening of population aging, the incidence of Alzheimer's disease is also on the rise, seriously affecting the quality of life of the elderly population. Therefore, the study of neuronal heat shock protein 70 and its ultrastructure is helpful to enhance the therapeutic effect and improve the quality of life of patients. To observe the effect of Zuogui pill on heat shock protein and ultrastructure of brain neurons in rats with Alzheimer's disease. The experimental rats were divided into model group, anti-cerebral failure control group, Haboin control group, Zuogui pill low-dose group, Zuogui pill high-dose group and sham operation group. The model group was injected with D-galactose intraperitoneal injection and amyloid-beta injection into the hippocampus to prepare an Alzheimer's disease animal model. The two control groups were injected with anti-Nao Shuai capsule and Haberman capsule while modeling. The sham operation group was injected with the same amount of normal saline into the hippocampus of both rats. After successful modeling, acetylcholinesterase of rat brain homogenate was detected by biochemical method, expression of heat shock protein 70 in hippocampus of rats in each group was measured by reverse transcription-polymerase chain reaction and ultrastructural changes of rat brain neurons were observed by transmission electron microscope. Zuogui pill could inhibit acetylcholinesterase activity, reduce apoptosis and stabilize the number of neurons. Ultrastructural observation also showed that hippocampal neurons in each treatment group showed morphological characteristics different from the early apoptosis in the model group. Zuogui pill has a positive effect on increasing the number of neurons surviving and inhibiting cell death. It can effectively promote the repair of nerve cells in the brain, thus improving memory impairment in Alzheimer's disease patients.