The Clinical Observation Of Bushenyijingfang For The Treatment Of Alzheimer’s Disease And D-Galactase-Induced Apoptosis Via MAPK Signaling Pathway In PC12 Cells

Objective:To explore the effect of Bushenyijingfang for treating Alzheimer’s disease in clinical and evaluate the effect of Bushenyijingfang on the D-galactase-induced apoptosis via MAPK signaling pathway in PC 12 cellsMethods:This research is divided into two parts:the first part is clinical cases observation, the plan is as follows:Research design follow block rule of double-blind, randomized, controlled, clinical collected 60 cases, randomly divided into two groups: treatment group Bushenyijingfang group and control groups Donepezil group, each group has 30 cases. The treatment group was given oral Bushenyijing decoction,200ml each time, two times a day.The control group was given oral donepezil,5mg each time, once a day.Observation period of the two groups was both six months.Six months later,calculated and compared TCM syndrome score, MMSE score and ADAS-cog score results to analysis the clinical efficacy before and after the treatment. The second part is the experimental research, the solution is as follows:First the rat adrenal pheochromocytoma (PC 12 cells) cells were cultived in vitro, and then added D-galactose for inducing PC 12 cell apoptosis and establishingthe model of Alzheimer’s disease. The experiments were divided into the following groups:the model group, the low, medium and high dose group of Bushenyijingfang, the inhibitor group of JNK, ERK and P38 MAPkinase, and the blank group without D-galactose, cultived for 24 h and 48 h, respectively, then detected and compared the Cell viability, cell apoptosis rate andAmount of protein expression in each group.Results:This study observed three indicators:MMSE score, ADAS-cog score and TCM syndrome score before and after the treatmentTCM syndrome score,MMSE score and ADAS-cog score before and after the treatment in the two groups showed statistically significant (P<0.05).The results showed that both the treatment group and the control group could improve the cognitive function and behavioral ability of patients with AD, and the treatment group in improving patient has the obvious advantage of TCM syndrome. Experimental results:l.cell viability:Compared with the blank group, the cell viability in the model group decreased significantly(P<0.01).Compared with the model group, the cell viability in the high dose group of Bushenyijingfang were significantly higher (P<0.05), the inhibitor group of P38MAPkinase were significantly higher (P<0.05).2. cell apoptosis rate:Compared with the blank group, the cell apoptosis rate in the model group increased significantly (P<0.001).Compared with the model group, the cell apoptosis rate in the high dose group of Bushenyijingfang were significantly lower (P<0.01), the inhibitorgroup of P38MAPkinase were significantly lower (P<0.01).3. amount ofprotein expression: Compared with the blank group, the amount of protein expression in the model group decreased significantly (P<0.05). The amount of phosphorylation protein expression of the inhibitor group of P38 MAPkinase in the high dose group of Bushenyijingfang were significantly decreased (P<0.001).The result indicate that the high dose group of Bushenyijingfang was able to ameliorate D-galactase-induced apoptosis in PC 12 cells via P38MAPK signaling pathway.Conclusion:Both Bushenyijingfang and donepezil displayed the same effect on the treatment of the cognitive function and behavioral ability of patients with AD. But the effect of Bushenyijingfang is better than donepezil in improving the TCM syndromes and no obvious adverse reaction.The results showed that Bushenyijingfang was able to ameliorate D-galactase-induced apoptosis in PC 12 cells. The protective effects of Bushenyijingfang were related to the inhibition of P38MAP kinase.