Alzheimer's disease (AD) is the most common neurodegenerative disease, severely reducing the cognitive level and life quality of patients. Byu dMar 25 (BM25) has been proved to have a therapeutic effect on AD. However, the pharmacological mechanism is still unclear. Therefore, this study aims to reveal the potential mechanism of BM25 affecting AD from the perspective of network pharmacology and experimental validation. The potential active ingredients of BM25 were obtained from the TCMSP database and literature. Possible targets were predicted using SwissTargetPrediction tools. AD-related genes were identified by using GeneCards, OMIM, DisGeNET, and Drugbank databases. The candidate genes were obtained by extraction of the intersection network. Additionally, the "drug-target-disease" network was constructed by Cytoscape 3.7.2 for visualization. The PPI network was constructed by the STRING database, and the core network modules were filtered by Cytoscape 3.7.2. Enrichment analysis of GO and KEGG was carried out in the Metascape platform. Ledock software was used to dock the critical components with the core target. Furthermore, protein levels were evaluated by immunohistochemistry. In this study, 112 active components, 1112 disease candidate genes, 3084 GO functions, and 277 KEGG pathways were obtained. Molecular docking showed that the effective components of BM25 in treating AD were β-asarone and hydroxysafflor yellow A. The most important targets were APP, PIK3R1, and PIK3CA. Enrichment analysis indicated that the Golgi genetic regulation, peroxidase activity regulation, phosphatidylinositol 3-kinase complex IA, 5-hydroxytryptamine receptor complexes, cancer pathways, and neuroactive ligand-receptor interactions played vital roles against AD. The rat experiment verified that BM25 affected PI3K-Akt pathway activation in AD. This study reveals the mechanism of BM25 in treating AD with network pharmacology, which provides a foundation for further study on the molecular mechanism of AD treatment.

Alzheimer’s disease is a common neurodegenerative disease in the elderly. This study explored the curative effect and possible mechanism of Acori graminei rhizoma on Alzheimer’s disease. In this paper, 8 active components of Acori graminei rhizoma were collected by consulting literature and using the TCMSP database, and 272 targets were screened using the PubChem and Swiss Target Prediction databases. Introduce it into the software of Cytoscape 3.7.2 and establish the graph of “drug‐active ingredient‐ingredient target.” A total of 276 AD targets were obtained from OMIM, Gene Cards, and DisGeNET databases. Import the intersection targets of drugs and diseases into STRING database for enrichment analysis, and build PPI network in the Cytoscape 3.7.2 software, whose core targets involve APP, AMPK, NOS3, etc. GO analysis and KEGG analysis showed that there were 195 GO items and 30 AD‐related pathways, including Alzheimer’s disease pathway, serotonin synapse, estrogen signaling pathway, dopaminergic synapse, and PI3K‐Akt signaling pathway. Finally, molecular docking was carried out to verify the binding ability between Acori graminei rhizoma and core genes. Our results predict that Acori graminei rhizoma can treat AD mainly by mediating Alzheimer’s signal pathway, thus reducing the production of Aβ, inhibiting the hyperphosphorylation of tau protein, regulating neurotrophic factors, and regulating the activity of kinase to change the function of the receptor.

Background: As the characteristics of the intertruncal approach to the supraclavicular block (IA-SCB) are uncertain, we aimed to compare its effect on sensory-motor blockade with that of the classical approach (CA) within 30 min post-block.Methods: In total, 122 patients undergoing elbow, forearm, wrist, or hand surgery were randomly assigned to receive CA-SCB or IA-SCB. Both groups received identical local anesthetic agents (1% lidocaine and 0.5% ropivacaine) in 25 ml total. The IA-SCB group received 15 ml between the middle and inferior trunks and 10 ml between the superior and middle trunks, while the CA-SCB group received 15 ml in the corner pocket and 10 ml in the center of the neural clusters. Sensory-motor blockade of all four terminal nerves was assessed every 5 min for 30 min. The non-inferiority threshold aimed to exclude the possibility that the IA-SCB was > 5% inferior to the CA-SCB in terms of the proportion of patients with complete sensory blockade at 20 min post-block.Results: Complete sensory blockade at 20 min post-block was 79.3% and 72.7% with the CA-SCB and IA-SCB, respectively, exceeding the non-inferiority margin of –5% (–6.6%, 95% CI [–22.3% to 9.1%]; P value for non-inferiority = 0.206). Additionally, the IA-SCB showed an inferior musculocutaneous nerve blockade, longer performance time, and higher incidence of hemidiaphragmatic paresis.Conclusions: Our findings do not confirm the non-inferiority of the IA-SCB to the CA-SCB in achieving complete sensory blockade at 20 min post-block. Further research may be necessary to establish its efficacy in regional anesthesia.