xCT Antibody - #DF12509

Fig. 3 PS-NPs initiate ferroptosis by triggering iron overload and ROS overproduction in GC-2 cells. (A) Various concentrations of PS-NPs (50 µg/mL, 100 µg/mL, 200 µg/mL) in different treatment times (6–24 h) reduce cell viability in GC-2 cells. (B and C) Representative images and quantification of fluorescence intensity for lipid peroxidation levels labelled with C11 BODIPY in GC-2 cells post-exposed with PS-NPs. Statistical analysis presented the ratio of MFI of green to red. (D-F) The levels of MDA, GSH, and total Fe were detected in GC-2 cells after PS-NPs treatment for 12 h. (G and H) Representative images and quantification of fluorescence intensity showing intracellular chelatable iron in GC-2 cells post-exposure to PS-NPs labelled with FerroOrange (red). (I and J) DCFH-DA staining was performed to detect ROS levels of GC-2 cells after PS-NPs exposure for 12 h using fluorescent microscopy. (K) Flow cytometry analysis of and ROS levels of GC-2 cells after PS-NPs exposure for 12 h using Fluorescence-activated cell sorting (FACS). (L) qRT-PCR analysis of ferroptosis-related gene expression in GC-2 cells treated with or without PS-NPs. (M and N) Ferroptosis-related proteins in GC-2 cells stimulated by PS-NPs were determined by western blotting. And semi-quantification of protein expression levels normalized to β-actin. (O) Representative TEM images depicting mitochondria in GC-2 cells in response to exposure to PS-NPs. The reduction of mitochondrial cristae is denoted by yellow arrows, while red arrows signify mitochondrial membrane rupture. (P and Q) Representative illustration and quantification of fluorescence intensity depicting mitochondria in GC-2 cells after treatment with PS-NPs using Mito-Tracker Green. (R and S) Illustration and quantification data of mitochondrial membrane potential in GC-2 cells in response to treatment of PS-NPs stained with TMRE

Fig. 3 PS-NPs initiate ferroptosis by triggering iron overload and ROS overproduction in GC-2 cells. (A) Various concentrations of PS-NPs (50 µg/mL, 100 µg/mL, 200 µg/mL) in different treatment times (6–24 h) reduce cell viability in GC-2 cells. (B and C) Representative images and quantification of fluorescence intensity for lipid peroxidation levels labelled with C11 BODIPY in GC-2 cells post-exposed with PS-NPs. Statistical analysis presented the ratio of MFI of green to red. (D-F) The levels of MDA, GSH, and total Fe were detected in GC-2 cells after PS-NPs treatment for 12 h. (G and H) Representative images and quantification of fluorescence intensity showing intracellular chelatable iron in GC-2 cells post-exposure to PS-NPs labelled with FerroOrange (red). (I and J) DCFH-DA staining was performed to detect ROS levels of GC-2 cells after PS-NPs exposure for 12 h using fluorescent microscopy. (K) Flow cytometry analysis of and ROS levels of GC-2 cells after PS-NPs exposure for 12 h using Fluorescence-activated cell sorting (FACS). (L) qRT-PCR analysis of ferroptosis-related gene expression in GC-2 cells treated with or without PS-NPs. (M and N) Ferroptosis-related proteins in GC-2 cells stimulated by PS-NPs were determined by western blotting. And semi-quantification of protein expression levels normalized to β-actin. (O) Representative TEM images depicting mitochondria in GC-2 cells in response to exposure to PS-NPs. The reduction of mitochondrial cristae is denoted by yellow arrows, while red arrows signify mitochondrial membrane rupture. (P and Q) Representative illustration and quantification of fluorescence intensity depicting mitochondria in GC-2 cells after treatment with PS-NPs using Mito-Tracker Green. (R and S) Illustration and quantification data of mitochondrial membrane potential in GC-2 cells in response to treatment of PS-NPs stained with TMRE