{Reference Type}: Journal Article
{Title}: Study of the multitarget mechanism of Astragalus (HUANGQI) in the treatment of Alzheimer's disease based on network pharmacology and molecular docking technology.
{Author}: Lv F;Sun M;Qin C;Du D;Zheng X;Li W;
{Journal}: Pharm Biol
{Volume}: 62
{Issue}: 1
{Year}: 2024 Dec
{Factor}: 3.889
{DOI}: 10.1080/13880209.2024.2382962
{Abstract}: <B>UNASSIGNED: </B>In China, HUANGQI is widely used for the treatment of Alzheimer's disease (AD). However, a comprehensive understanding of its mechanism of anti-AD effects is lacking.<BR><B>UNASSIGNED: </B>To explore the active ingredients of HUANGQI and its potential targets and mechanisms of action in AD.<BR><B>UNASSIGNED: </B>The active ingredients and targets of HUANGQI were screened from databases (TCSMP, ETCM, and BATMan), and AD-related genes were obtained from DrugBank and GeneCards. The same target genes were screened, and a drug-target disease network was constructed. The PPI network was constructed and GO and KEGG pathway enrichment analyses of the targets. The Cell Counting Kit-8 (CCK-8) assay was used to determine suitable HUANGQI treatment concentrations for HT-22 cells between 0-480 μg/mL. CCK-8, FITC-phalloidin and propidium iodide (PI) assays were used to examine the protective effect of (0, 60, 120, 240 μg/mL) of HUANGQI on 20 μM Aβ1-42-induced HT-22 cell cytotoxicity.<BR><B>UNASSIGNED: </B>Twelve active ingredients of HUANGQI were selected, with 679 common targets associated with AD. GO and KEGG analysis revealed that the therapeutic mechanisms of HUANGQI involve TNF, AGE, the NF-κB pathway, and nuclear receptor activity-related processes. The CCK-8 assay indicated that HUANGQI was not cytotoxic to HT-22 cells at concentrations less than 240 μg/mL and was able to attenuate Aβ1-42-induced cellular damage (EC50 = 83.46 μg/mL). FITC-phalloidin and PI assays suggested that HUANGQI could alleviate 20 μM Aβ1-42-induced neuronal cell cytotoxicity in a dose-dependent manner.<BR><B>UNASSIGNED: </B>HUANGQI has a protective effect on Aβ1-42-induced nerve cell injury; further mechanism research was needed.