Biomedicine & Pharmacotherapy, Journal Year: 2024, Volume and Issue: 182, P. 117769 - 117769
Published: Dec. 16, 2024
Language: Английский
Biomedicine & Pharmacotherapy, Journal Year: 2024, Volume and Issue: 182, P. 117769 - 117769
Published: Dec. 16, 2024
Language: Английский
Journal of Contemporary Medical Practice, Journal Year: 2025, Volume and Issue: 7(1), P. 201 - 211
Published: Jan. 31, 2025
Background: Fucoxanthin (Fx) is a natural carotenoid gaining widespread interest for its anticancer effects. However, the mechanism by which Fx treats leukemia remains unclear. Here, we studied of Fx-induced ferroptosis in human erythroleukemia (HEL) cells. Methods: HEL cell viability after treatment was assessed using an MTT assay. Mitochondrial membrane potential (MMP) and cycle distribution cells were determined flow cytometry. Fucoxanthin's effect on reactive oxygen species (ROS), iron ferrous ions measured assay kits. Expression levels relevant proteins through western blot analysis. Molecular docking performed to validate interactions. Results: significantly inhibited both dose- time-dependently. As concentration increased, proportion G0/G1 phase MMP S notably decreased. markedly promoted ROS, ion expression levels; reduced GPX4 SCL7A11 levels, increased p53 TFR1 levels. analysis revealed that binding energy between GPX4, SCL7A11, less than −5 kcal/mol, primarily hydrogen bonding at enzyme's active site. Conclusion: may be related activation TFR1/SLC7A11/GPX4 signaling pathway.
Language: Английский
Citations
0Biomedicine & Pharmacotherapy, Journal Year: 2024, Volume and Issue: 182, P. 117769 - 117769
Published: Dec. 16, 2024
Language: Английский
Citations
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