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Objective:To investigate the efficacy of galantamine combined with Fufang Haishe Jiaonang in the treatment of Alzheimer's disease and its effects on serum levels of inflammatory factors, Aβ1-42 protein, and Tau protein. Methods:A total of 104 patients with Alzheimer's disease who received treatment in Jiaozhou People's Hospital from January 2019 to January 2021 were included in this study. They were randomly divided into a control group and an observation group ( n = 52/group). The control group was given galantamine treatment. The observation group was given galantamine combined with Fufang Haishe Jiaonang. All patients were treated for 3 months. Clinical efficacy was compared between the two groups. Before and after treatment, serum inflammatory factor, Aβ1-42 protein, Tau protein, Mini-Mental State Examination score, and The Quality of Life in Alzheimer's Disease Seale score were compared between the two groups. Adverse reactions were observed during the treatment. Results:Total response rate in the observation group was significantly higher than that in the control group [92.31% (48/52) vs. 76.92% (40/52), χ2 = 4.73, P < 0.05]. After treatment, serum levels of interleukin-6, interleukin-8, tumor necrosis factor-alpha, and Tau protein in the observation group were significantly lower than those in the control group, and Aβ1-42 protein level in the observation group was significantly higher than that in the control group ( t = 16.78, 6.94, 5.16, 2.91, 2.55, all P < 0.05). After treatment, Mini-Mental State Examination score and The Quality of Life in Alzheimer's Disease (QOL-AD) Seale score were increased in each group ( t = 13.48, 6.34, 18.58, 14.45, all P < 0.001), and they were significantly higher in the observation group than the control group ( t = 5.86, 7.25, both P < 0.05). There was no significant difference in the incidence of adverse reactions between the two groups ( P > 0.05). Conclusion:Galantamine combined with Fufang Haishe Jiaonang for the treatment of Alzheimer's disease can better reduce clinical symptoms and signs, regulate serum levels of inflammatory factors, Aβ1-42 protein, and Tau protein, and improve the mental state and quality of life.
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OBJECTIVE：To study the improvement effects of sinapic acid （SA）on PC 12 cell damage induced by Aβ1-42，and to investigate its effect on brain-derived neurotrophic factor （BDNF）/tyrosine kinase B （TrkB）/extracellular signal-regulated kinase （ERK）signaling pathway. METHODS ：PC12 cells were divided into blank group ，model group ，SA low-dose and high-dose groups（50，100 μmol/L）. Except for blank group ，cell damage was induced by Aβ1-42 in other groups ；24 h after modeling ， administration groups were added with the corresponding solution and cultured for 24 h. Morphological changes of cells in each group were observed. Cell survival rate ，mRNA expression and protein level of BDNF ，protein expression of TrkB ，ERK1/2 and phosphorylated ERK 1/2（p-ERK1/2）were detected. p-ERK/ERK ratio was calculated. RESULTS ：Compared with blank group ，the model group had shorter synapses ，looser intercellular junctions ，poor adhesion ，dim cytoplasm and more granules in cytoplasm. Cell survival rate and mRNA expression and protein level of BDNF ，the relative expression of TrkB and p-ERK 1/2 protein，p-ERK/ ERK ratio were significantly decreased （P＜0.05 or P＜0.01）. Compared with model group ，in SA high-dose group the pathological changes of the cells were significantly improved ，the survival rate of the cells ，the mRNA expression and protein level of BDNF，the relative expression of TrkB and p-ERK 1/2 protein， p-ERK/ERK ratio were significantly increased （P＜0.05 or P＜ 0.01）. CONCLUSIONS：SA can i mprove PC 12 cells damage induced by Aβ1-42，the mechanism of which may be associated with activating BDNF/TrkB/ERK signaling pathway. qq.com