ArticleNaunyn-Schmiedeberg's archives of pharmacology2026
Phytochemical characterization and multi-target mechanism of Gleditsia sinensis Fructus in lung adenocarcinoma treatment.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Gleditsia sinensis Fructus (GSF) exhibits anti-cancer activity and is effective against lung adenocarcinoma (LUAD). However, its underlying mechanisms remain unclear. In this study, the potential chemical components, targets, and pathways of GSF in treating LUAD were investigated using UHPLC-HRMS combined with network pharmacology analysis. These findings were subsequently verified via molecular docking, molecular dynamics simulation, and in vitro cell experiments. The results showed that a total of 61 components targeting 192 LUAD-related genes were identified, and 177 candidate targets of GSF against LUAD were obtained, among which AKT1, SRC, EGFR, IL6, and TNF may be the core targets. Enrichment analysis revealed that the mechanisms were related to various cancer-related pathways, particularly the PI3K-AKT signaling pathway. Molecular docking demonstrated that the active components of GSF, particularly luteolin, exhibited excellent binding affinity to the top five core targets. Molecular dynamics simulation results showed a similar trend. Therefore, we identified luteolin as the primary active component of GSF. The cell experiments revealed that luteolin significantly inhibited cell growth and proliferation and promoted the apoptosis of A549 cells, exhibiting effects similar to those of cisplatin. In addition, luteolin significantly upregulated the expression of Bax and cleaved-caspase3 and decreased the expression of P-AKT and BCL2. Our results demonstrate that GSF can exert anti-LUAD effects through multi-components, multi-targets, and multi-pathways. Luteolin, one of the main active components of GSF, suppressed proliferation and induced apoptosis in A549 cells, possibly through inhibiting the AKT signaling pathway.
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