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Objective @#To investigate the effects of cynomorium songaricum extract on cognitive dysfunction of Alzheimer disease (AD) model mice based on network pharmacology and animal experiments.@*Methods @#Network pharmacology was used to predict the related targets and signal pathways of the extract of cynomorium songaricum to improve AD. Senescence accelerated mice P8 (SAMP8) were selected as the model of AD. Based on the results of the preliminary experiment , 0. 17 g/(kg ·d) was selected as the optimal dosage for the extract of cynomorium songaricum. The extract of cynomorium songaricum [0. 17 g/(kg ·d) , Donepezil hydrochloride [2. 0 mg/(kg ·d)] and normal saline were given orally for 28 days according to the groups. Morris water maze evaluated the learning and cognitive function of animals. The number of neurons in cornu ammonis 1 (CA1) of hippocampus was ob served by Nissl staining. The expression of recombinant Beclin 1(Beclin ⁃1) , Sequestosome 1 (p62) , light chain 3 (LC⁃ nase (PI3K) , protein kinase B (AKT) and glycogen synthase kinase3β (GSK⁃3β) in the hippocampus of mice in each group were detected by Western blot.@*Results @#Based on the network pharmacology study , it was predicted that the biological mechanism of cynomorium songaricum to improve AD might be the regulation of autophagy , and the possible signaling pathway was PI3K/AKT/GSK⁃3β . The results of animal experiments showed that the extract age of hippocampal neurons , significantly increase the number of neurons , and increase the expression levels of PI3K , p ⁃AKT/AKT , p ⁃GSK⁃3β/GSK⁃3β , B eclin ⁃1 and LC3 in the hippocampus of mice. The expression level of p62 decreased. There was no significant difference between male and female mice during the experiment. @*Conclusion@#The extract may improve the cognitive dysfunction of male and female AD models by activating autophagymediated by PI3K⁃AKT⁃GSK⁃3β signaling pathway , and there is no significant gender difference in the effect.
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[ ABSTRACT] AIM:To investigate the inhibitory effect of Am80 on neointima hyperplasia in carotid arteries after balloon injury and to observe the interaction between Krüppel-like factor 4 (KLF4) and retinoic acid receptorα(RARα). METHODS:Neointima hyperplasia in carotid arteries was observed by hemotoxylin and eosin staining.The expression of KLF4 and cyclin D1 was examined by immunostaining and Western blotting analysis.To detect the interaction between KLF4 and RARαin the vascular tissue, the injured arteries were harvested, and the protein extracts were prepared and subjected to co-immunoprecipitation assay.RESULTS:Compared with injured group, Am80 significantly reduced neointi-mal hyperplasia and the thickness ratio of intima to media.Am80 not only up-regulated KLF4 or RARαexpression in caro-tid arteries, but also increased the interaction between KLF4 and RARαat tissue levels.CONCLUSION:Am80 inhibits neointima hyperplasia in carotid arteries after balloon injury by promoting the interaction between KLF4 and RARα.