Journal of chromatography. B, Analytical technologies in the biomedical and life sciences · 2026
Deficiency in beclin1 alleviates doxorubicin-induced liver injury through inhibiting ferroptosis and autophagy.
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Zhang Linlin, He Yuying, Zhao Anbo, Han Hui, Li Yuping, Li Lu, Zhang Yuming, Gao Qin, Ye Hongwei
Аннотация
OBJECTIVES: Doxorubicin (DOX) is an effective chemotherapy drug, but it has severe hepatotoxicity. Ferroptosis is one of the main mechanisms of DOX-induced liver injury. Beclin1 is a core molecule in regulating autophagy, and it has also been reported to be involved in the regulation of ferroptosis. We aimed to study the role of Beclin1 in DOX-induced liver ferroptosis and autophagy.
METHODS: DOX was used to induce liver injury and AML-12 liver cell injury. The morphological alterations in liver tissues were detected by hematoxylin and eosin staining. The levels of malondialdehyde, superoxide dismutase, alanine aminotransferase, aspartate aminotransferase, and Fe2+ were detected by the related kits. The level of reactive oxygen species was detected by dihydroethidium. The level of lipid peroxidation was detected by C11-BODIPY. The protein expression of Beclin1 and dihydroorotate dehydrogenase (DHODH) was detected by immunofluorescence. The interactions between different proteins were predicted by molecular docking. The interaction between Beclin1 and DHODH was detected by co-immunoprecipitation. Beclin1, sequestosome-1 (p62), microtubule-associated protein 1 light chain 3B (LC3B), DHODH, glutathione peroxidase 4 (GPX4), ferroptosis suppressor protein 1 (FSP1), Nuclear Receptor Coactivator 4 (NCOA4), and Ferritin Heavy Chain 1 (FTH1), protein expression levels were detected by western blotting.
RESULTS: Ferroptosis and autophagy both occur in DOX-induced liver injury. Beclin1 knockdown decreased hepatic oxidative stress and inhibited ferroptosis and autophagy. DHODH overexpression decreased hepatic oxidative stress and inhibited ferroptosis and autophagy.
CONCLUSION: Beclin1 knockdown and DHODH overexpression can reduce DOX-induced liver injury by preventing ferroptosis and autophagy.
METHODS: DOX was used to induce liver injury and AML-12 liver cell injury. The morphological alterations in liver tissues were detected by hematoxylin and eosin staining. The levels of malondialdehyde, superoxide dismutase, alanine aminotransferase, aspartate aminotransferase, and Fe2+ were detected by the related kits. The level of reactive oxygen species was detected by dihydroethidium. The level of lipid peroxidation was detected by C11-BODIPY. The protein expression of Beclin1 and dihydroorotate dehydrogenase (DHODH) was detected by immunofluorescence. The interactions between different proteins were predicted by molecular docking. The interaction between Beclin1 and DHODH was detected by co-immunoprecipitation. Beclin1, sequestosome-1 (p62), microtubule-associated protein 1 light chain 3B (LC3B), DHODH, glutathione peroxidase 4 (GPX4), ferroptosis suppressor protein 1 (FSP1), Nuclear Receptor Coactivator 4 (NCOA4), and Ferritin Heavy Chain 1 (FTH1), protein expression levels were detected by western blotting.
RESULTS: Ferroptosis and autophagy both occur in DOX-induced liver injury. Beclin1 knockdown decreased hepatic oxidative stress and inhibited ferroptosis and autophagy. DHODH overexpression decreased hepatic oxidative stress and inhibited ferroptosis and autophagy.
CONCLUSION: Beclin1 knockdown and DHODH overexpression can reduce DOX-induced liver injury by preventing ferroptosis and autophagy.