动物造模 Z-bio 2023-01-29 357

　　Objective To investigate the effect of Kaixinsan on the injection of A into bilateral hippocampal CA1 region β The therapeutic effect of 1-42 on AD rats, and its mechanism of action is preliminarily clarified.

　　Method with“ β- According to the theory of amyloid protein toxicity ", inject A into the CA1 area of bilateral hippocampus of SD rats using brain stereotaxic apparatus β 1-42 oligopeptide segment to replicate AD rat model. Dementia rats were randomly divided into model group, huperzine A group, Kaixinsan low dose group, middle dose group and high dose group, with 10 rats in each group. Another 10 rats were injected with the same amount of normal saline into the brain as the sham operation group, and 10 normal rats as the blank control group. Continuous intragastric administration for 30 days. The changes of learning and memory performance of rats were observed by Morris water maze behavioral test; HE staining and Nissl staining were used to observe the pathological morphology of brain tissue; Detection of cholinergic neurotransmitters (ACh, AChE, ChAT) and inflammatory factors (TNF) in brain tissue by ELISA- α、 IL-6、 IL-1 β) And β- Amyloid protein (APP, A β 1-40 、A β 1-42); IHC analysis of tau protein and GSK-3 in cortex and hippocampus β Expression level of; Western blot was used to observe the expression of BAX and BCL-2 in brain tissue.

　　Results Compared with the model group, the escape latency of rats in the Kaixinsan intervention group was significantly shortened, the number of times of crossing the platform was increased, and the percentage of staying time and swimming distance in the target quadrant were increased (P<0.05) 05 or P<0 01); The number of neurons in cortex and hippocampus increased, the morphology and structure tended to be normal, and the number of Nissan bodies increased, and the cytoplasmic staining deepened; The activity of AChE in brain tissue decreased, and the contents of ChAT and ACh increased significantly (P<0.05) 05 or P<0 01); TNF- α、 IL-6、IL-1 β、 APP、A β 1-40 and A β The content of 1-42 decreased significantly (P<0.01) 05 or P<0 01); Tau protein and GSK-3 in cortex and hippocampus β The positive expression of β - lactamase was down-regulated (P<0.05) 05 or P<0 bax="" bcl-2="" p="">0. 05)。

　　Conclusion Kaixin powder has a good therapeutic effect on dementia symptoms and brain tissue injury in AD injured rats. Its mechanism involves the repair of cholinergic system, the inhibition of inflammatory factor release β- The clearance of amyloid protein and the regulation of tau protein phosphorylation level.