Effects And Mechanisms Of The Shenghui Keli On Alzheimer's Disease Rats Induced By β-Amyloid Protein

Objective To observe the effect of Shenghui Keli on AD (Alzheimer's disease) encephalon neural degeneration induced by A β (β -Amyloid protein) from neural function, biochemical and gene expression. Research the degeneration related to apoptosis of cell and gene expression correlate to apoptosis. Then investigate the mechanisms of Shenghui keli treating AD .Methods Animal models of AD was successfully induced in rats by trace injection of A β on basal nuclei, the rats were divided into AD model group, Shenghui Keli treatment group of high dose, middle dose, low dose and Nimodipine positive control group; normal control group was another group of 30 normal rats, which was injected with sodium chloride. The rats were given correspondence drug once a day (normal control group and model group were given with saline). Y maze experiments were carried out at 15th, 30th day to study the rats' skill of learn and memory. After 30 days treatment, rats heart were instilled in vivo with 4% Citromint after anesthesia. Hippocampus paraffin section was made to observe the HE staining and TUNEL staining. Thecondition of Fresh hippocampus apoptosis was observed by electron microscope, extracting DNA to observe agarose caraphoresis. Meanwhile, the expression of Bax and Bcl-2 proteins was detected by immunohistochemistry and quantified by using computerized image analysis.Results It was found that the try number of times of AD model group was significantly increased, which indicated the AD model group existed disability of learn and memory and had noticeable difference to normal group (P<0.01). From the result of HE staining, we found that the AD model group hippocampus cell was degenerated, but the hippocampus cell degeneration of Shenghui keli group and positive group decreased significantly (P<0.01). The AD model group was detected characteristic of apoptosis by TUNEL staining, DNA electrophoresis and electron microscope. Compared with that in normal control group, the expression of Bax was significantly increased (P <0.01), but the expression of Bcl-2 was significantly decreased in AD rats model (P <0.01). Compared with that in AD model, the expression of Bax was significantly lower than it (P <0.01), and the expression of Bcl-2 was not significantly different in hippocampus in Shenghui Keli group and positive group (P>0.05). The ratio of Bax to Bcl-2 was significantly decreased in hippocampus (P <0.01).Conclusion It was found that the disability of learn and memory can be observed by trace injection of A β on basal nuclei, which also could be observed the degeneration and characteristic ofapoptosis. The expression of Bax was significantly higher, and the expression of Bcl-2 was lower than it, the ratio of Bax to Bcl-2 was significantly increased in hippocampus the rats with AD. Shenghui Keli could treat AD, promoting the skill of learn and memory of AD rats induced by A β ; reliving the rat hippocampus cell lesion, inhibiting the apoptosis of cells, control the Bax,Bcl-2 expression relate to apoptosis .