文献类型：期刊文献

英文题名：Agaricus blazei Murill Extract (FA-2-b-β) Induces Ferroptosis in Diffuse Large B-Cell Lymphoma via the Nrf2/Ho-1 Pathway

作者：Li, Rong[1];Huang, Dan[1];Wu, Along[1];Sun, Yanqin[1,2]

第一作者：李融

通信作者：Sun, YQ[1]

机构：[1]Gansu Univ Chinese Med, Clin Coll 1, Lanzhou 734000, Gansu, Peoples R China;[2]Gansu Prov Hosp, Dept Hematol, Lanzhou 734000, Gansu, Peoples R China

第一机构：甘肃中医药大学

通信机构：[1]corresponding author), Gansu Prov Peoples Hosp, 204 Donggang West Rd, Lanzhou 734000, Gansu, Peoples R China.

年份：2025

外文期刊名：COMBINATORIAL CHEMISTRY & HIGH THROUGHPUT SCREENING

收录：;Scopus(收录号：2-s2.0-105001712211);WOS:【SCI-EXPANDED(收录号:WOS:001444652600001)】；

基金：This study was supported by the Gansu Provincial People's Hospital Outstanding Master's/Doctoral Student Cultivation Program (No. ZX-62000001-2022-678) and the Gansu Provincial Department of Education Excellent Graduate "Innovation Star" Project (No. 2023CXZX-757).

语种：英文

外文关键词：FA-2-b-beta; diffuse large B-cell lymphoma; ferroptosis

摘要：Introduction Ferroptosis is a recently identified iron-dependent programmed cell death closely linked to the progression of diffuse large B-cell lymphoma (DLBCL). While studies have shown that FA-2-b-beta extracted from Agaricus blazei Murill affects various malignancies, its specific role in modulating ferroptosis in DLBCL and the underlying mechanisms are not yet clear. Objectives: This study aims to elucidate the anticancer properties and mechanisms of FA-2-b-beta in inducing ferroptosis in DLBCL cells.Methods The cell counting kit 8 assay was carried out to evaluate the inhibition of cellular proliferation. Ferroptosis was evaluated using the ferrous colorimetric method, together with kits for measuring malondialdehyde (MDA), reduced glutathione (GSH), reactive oxygen species (ROS), western blotting, JC-1 assays, and transmission electron microscopy. Reverse transcription-quantitative polymerase chain reaction and western blot were conducted to determine whether FA-2-b-beta affected nuclear factor erythroid 2- related factor 2 (Nrf2) and heme oxygenase 1 (HO-1).Results FA-2-b-beta induced ferroptosis in DLBCL cells by elevating the ROS and MDA levels, facilitating the accretion of Fe2+, diminishing GSH, upregulating the expression of PTGS2, and downregulating the expression of FTH1, SLC7A11, and GPX4. Furthermore, FA-2-b-beta caused structural damage to mitochondria and diminished the mitochondrial membrane potential. The ferroptosis triggered by FA-2-b-beta also led to the downregulation of Nrf2 and HO-1, thereby regulating the Nrf2/HO-1 pathway.Conclusion FA-2-b-beta suppressed DLBCL cell growth by inducing ferroptosis through the Nrf2/HO-1 pathway, making it an attractive potential therapeutic option.