Naringenin alleviates liver ﬁbrosis by triggering autophagy-dependent ferroptosis in hepatic stellate cells

Yu, Ting; Lu, Xuejia; Liang, Yan; Yang, Lin; Yin, Yuehan; Chen, Hong

doi:10.1016/j.heliyon.2024.e28865

Cited by 2 publications

(1 citation statement)

References 52 publications

(57 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…There is increasing evidence that ferroptosis plays an important role in regulating the occurrence and progression of various diseases. For example, hepatocytes exhibit key characteristics of ferroptosis during acute liver injury [ 14 ]. The morphological appearance of ferroptosis comprises shrunken mitochondria, increased mitochondrial membrane density, reduced or absent mitochondrial cristae, and rupture of the outer mitochondrial membrane.…”

Section: Introductionmentioning

confidence: 99%

Fucoxanthin Induces Ferroptosis in Cancer Cells via Downregulation of the Nrf2/HO−1/GPX4 Pathway

Du,

Wu,

Zhu

et al. 2024

Molecules

View full text Add to dashboard Cite

This study investigated the mechanism by which fucoxanthin acts as a novel ferroptosis inducer to inhibit tongue cancer. The MTT assay was used to detect the inhibitory effects of fucoxanthin on SCC−25 human tongue squamous carcinoma cells. The levels of reactive oxygen species (ROS), mitochondrial membrane potential (MMP), glutathione (GSH), superoxide dismutase (SOD), malondialdehyde (MDA), and total iron were measured. Reverse transcription–quantitative polymerase chain reaction (RT−qPCR) and Western blotting were used to assess glutathione peroxidase 4 (GPX4), nuclear factor erythroid 2−related factor 2 (Nrf2), Keap1, solute carrier family 7 member 11 (SLC7A11), transferrin receptor protein 1 (TFR1), p53, and heme oxygenase 1 (HO−1) expression. Molecular docking was performed to validate interactions. Compared with the control group, the activity of fucoxanthin−treated SCC−25 cells significantly decreased in a dose− and time−dependent manner. The levels of MMP, GSH, and SOD significantly decreased in fucoxanthin−treated SCC−25 cells; the levels of ROS, MDA, and total iron significantly increased. mRNA and protein expression levels of Keap1, GPX4, Nrf2, and HO−1 in fucoxanthin−treated cells were significantly decreased, whereas levels of TFR1 and p53 were significantly increased, in a concentration−dependent manner. Molecular docking analysis revealed that binding free energies of fucoxanthin with p53, SLC7A11, GPX4, Nrf2, Keap1, HO−1, and TFR1 were below −5 kcal/mol, primarily based on active site hydrogen bonding. Our findings suggest that fucoxanthin can induce ferroptosis in SCC−25 cells, highlighting its potential as a treatment for tongue cancer.

show abstract

Section: Introductionmentioning

confidence: 99%