文献类型：期刊文献

英文题名：Network Pharmacology and In Vitro Experiments Reveal the Mechanism of Agaricus blazei Murill Extract in Treating Chronic Myeloid Leukemia

作者：Wang, Dongping[1,2];Zhu, Hongwen[3];Ge, Wanwen[3];Sun, Yanqing[1,2]

第一作者：Wang, Dongping

通信作者：Sun, YQ[1];Sun, YQ[2];Ge, WW[3]

机构：[1]Gansu Univ Chinese Med, Lanzhou, Peoples R China;[2]Gansu Prov Hosp, Lanzhou, Peoples R China;[3]Lanzhou Univ Second Hosp, Cuiying Biomed Res Ctr, Lanzhou, Peoples R China

第一机构：甘肃中医药大学

通信机构：[1]corresponding author), Gansu Univ Chinese Med, Lanzhou, Peoples R China;[2]corresponding author), Gansu Prov Hosp, Lanzhou, Peoples R China;[3]corresponding author), Lanzhou Univ Second Hosp, Cuiying Biomed Res Ctr, Lanzhou, Peoples R China.|[10735]甘肃中医药大学;

年份：2025

外文期刊名：CHEMISTRY & BIODIVERSITY

收录：;Scopus(收录号：2-s2.0-105011985826);WOS:【SCI-EXPANDED(收录号:WOS:001536272600001)】；

基金：This work was financially supported by the Natural Science Foundation of China (32260151) and the Natural Science Foundation of Gansu Province(22JR5RA981, 206064305045).

语种：英文

外文关键词：chronic myeloid leukemia; experimental validation; FA-2-b-beta; liquid chromatography-tandem mass spectrometry (LC-MS/MS); network pharmacology

摘要：Chronic myeloid leukemia (CML) is a malignant hematological neoplasm. FA-2-b-beta, extracted from Agaricus blazei Murrill, has demonstrated antitumor activity against multiple cancer types. Nevertheless, the specific pharmacodynamic components and molecular mechanisms of FA-2-b-beta against CML remain to be elucidated. This study aimed to systematically investigate the mechanism of FA-2-b-beta against CML through an integrated strategy combining liquid chromatography-tandem mass spectrometry (LC-MS/MS), network pharmacology prediction, and in vitro experimental validation. Using LC-MS/MS profiling, we identified a total of 126 chemical components. Subsequently, network pharmacological analysis screened 45 potentially active components and 129 CML-related overlapping targets. Further pathway enrichment analysis revealed that these candidate targets were predominantly involved in the PI3K/AKT and MAPK pathways. In vitro validation confirmed the suppression of PI3K/AKT phosphorylation in K562 cells. Collectively, this study provides significant insights into the active components and antitumor mechanisms of FA-2-b-beta, emphasizing its potential as a promising therapeutic agent for treating CML.