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A The schema illustrates primary hepatocytes isolated from WT and Orm2 -/- mice, then treated with FINO2 or RSL3, with cell survival, cell death, ferrous iron, and lipid peroxidation levels measured. B WT and Orm2 -/- primary hepatocytes were treated with indicated doses of FINO2 for 12 h, cell viability was measured using CCK8. C WT and Orm2 -/- primary hepatocytes were treated with 8 μM FINO2 for 12 h, and <t>propidium</t> iodide (PI) staining to assess cell death. Quantification on the right. Scale bar, 100 μm. D – E WT and Orm2 -/- primary hepatocytes were treated with 8 μM FINO2 for 3 h, Fe 2+ levels and lipid peroxidation were visualized using FerroOrange and C11-BODIPY staining respectively. Scale bar, 100 µm. F The schema illustrates HepG2 cells with ORM2 knockdown, cells were treated with FINO2 or RSL3, with cell survival, cell death, ferrous iron, and lipid peroxidation levels measured. G HepG2 cells with ORM2 knockdown were treated with FINO2 at the indicated concentrations for 12 h, and cell viability was assessed using CCK8. H HepG2 cells with ORM2 knockdown were treated with 8 μM FINO2 for 12 h, PI staining was measured. Quantification on the right. Scale bar, 100 μm. I – J HepG2 cells with ORM2 knockdown were treated with 8 μM FINO2 for 3 h, Fe 2+ levels and lipid peroxidation were visualized using FerroOrange and C11-BODIPY staining respectively. Scale bar, 100 μm. K Flag-ORM2 was overexpressed into HepG2 cells, cells were treated with FINO2 at indicated doses for 12 h. Cell viability was assessed using CCK8. L HepG2 cells with ORM2 overexpressing were treated with 8 μM FINO2 for 12 h, PI staining was measured. Quantification on the right. Scale bar, 100 μm. M – N HepG2 cells with ORM2 overexpressing were treated with 8 μM FINO2 for 3 h, Fe 2+ levels and lipid peroxidation were visualized using FerroOrange and C11-BODIPY staining, respectively. Scale bar, 100 μm. All data in this figure are represented as mean ± SEM. Data were analyzed by two-way ANOVA followed by Bonferroni’s multiple comparisons test for comparisons between genotypes. Exact p values are provided in the figure. All experiments were performed in triplicates.
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A The schema illustrates primary hepatocytes isolated from WT and Orm2 -/- mice, then treated with FINO2 or RSL3, with cell survival, cell death, ferrous iron, and lipid peroxidation levels measured. B WT and Orm2 -/- primary hepatocytes were treated with indicated doses of FINO2 for 12 h, cell viability was measured using CCK8. C WT and Orm2 -/- primary hepatocytes were treated with 8 μM FINO2 for 12 h, and <t>propidium</t> iodide (PI) staining to assess cell death. Quantification on the right. Scale bar, 100 μm. D – E WT and Orm2 -/- primary hepatocytes were treated with 8 μM FINO2 for 3 h, Fe 2+ levels and lipid peroxidation were visualized using FerroOrange and C11-BODIPY staining respectively. Scale bar, 100 µm. F The schema illustrates HepG2 cells with ORM2 knockdown, cells were treated with FINO2 or RSL3, with cell survival, cell death, ferrous iron, and lipid peroxidation levels measured. G HepG2 cells with ORM2 knockdown were treated with FINO2 at the indicated concentrations for 12 h, and cell viability was assessed using CCK8. H HepG2 cells with ORM2 knockdown were treated with 8 μM FINO2 for 12 h, PI staining was measured. Quantification on the right. Scale bar, 100 μm. I – J HepG2 cells with ORM2 knockdown were treated with 8 μM FINO2 for 3 h, Fe 2+ levels and lipid peroxidation were visualized using FerroOrange and C11-BODIPY staining respectively. Scale bar, 100 μm. K Flag-ORM2 was overexpressed into HepG2 cells, cells were treated with FINO2 at indicated doses for 12 h. Cell viability was assessed using CCK8. L HepG2 cells with ORM2 overexpressing were treated with 8 μM FINO2 for 12 h, PI staining was measured. Quantification on the right. Scale bar, 100 μm. M – N HepG2 cells with ORM2 overexpressing were treated with 8 μM FINO2 for 3 h, Fe 2+ levels and lipid peroxidation were visualized using FerroOrange and C11-BODIPY staining, respectively. Scale bar, 100 μm. All data in this figure are represented as mean ± SEM. Data were analyzed by two-way ANOVA followed by Bonferroni’s multiple comparisons test for comparisons between genotypes. Exact p values are provided in the figure. All experiments were performed in triplicates.
Acridine Orange Propidium Iodide Ao Pi Double Staining Kit, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 98/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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A The schema illustrates primary hepatocytes isolated from WT and Orm2 -/- mice, then treated with FINO2 or RSL3, with cell survival, cell death, ferrous iron, and lipid peroxidation levels measured. B WT and Orm2 -/- primary hepatocytes were treated with indicated doses of FINO2 for 12 h, cell viability was measured using CCK8. C WT and Orm2 -/- primary hepatocytes were treated with 8 μM FINO2 for 12 h, and <t>propidium</t> iodide (PI) staining to assess cell death. Quantification on the right. Scale bar, 100 μm. D – E WT and Orm2 -/- primary hepatocytes were treated with 8 μM FINO2 for 3 h, Fe 2+ levels and lipid peroxidation were visualized using FerroOrange and C11-BODIPY staining respectively. Scale bar, 100 µm. F The schema illustrates HepG2 cells with ORM2 knockdown, cells were treated with FINO2 or RSL3, with cell survival, cell death, ferrous iron, and lipid peroxidation levels measured. G HepG2 cells with ORM2 knockdown were treated with FINO2 at the indicated concentrations for 12 h, and cell viability was assessed using CCK8. H HepG2 cells with ORM2 knockdown were treated with 8 μM FINO2 for 12 h, PI staining was measured. Quantification on the right. Scale bar, 100 μm. I – J HepG2 cells with ORM2 knockdown were treated with 8 μM FINO2 for 3 h, Fe 2+ levels and lipid peroxidation were visualized using FerroOrange and C11-BODIPY staining respectively. Scale bar, 100 μm. K Flag-ORM2 was overexpressed into HepG2 cells, cells were treated with FINO2 at indicated doses for 12 h. Cell viability was assessed using CCK8. L HepG2 cells with ORM2 overexpressing were treated with 8 μM FINO2 for 12 h, PI staining was measured. Quantification on the right. Scale bar, 100 μm. M – N HepG2 cells with ORM2 overexpressing were treated with 8 μM FINO2 for 3 h, Fe 2+ levels and lipid peroxidation were visualized using FerroOrange and C11-BODIPY staining, respectively. Scale bar, 100 μm. All data in this figure are represented as mean ± SEM. Data were analyzed by two-way ANOVA followed by Bonferroni’s multiple comparisons test for comparisons between genotypes. Exact p values are provided in the figure. All experiments were performed in triplicates.
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A The schema illustrates primary hepatocytes isolated from WT and Orm2 -/- mice, then treated with FINO2 or RSL3, with cell survival, cell death, ferrous iron, and lipid peroxidation levels measured. B WT and Orm2 -/- primary hepatocytes were treated with indicated doses of FINO2 for 12 h, cell viability was measured using CCK8. C WT and Orm2 -/- primary hepatocytes were treated with 8 μM FINO2 for 12 h, and <t>propidium</t> iodide (PI) staining to assess cell death. Quantification on the right. Scale bar, 100 μm. D – E WT and Orm2 -/- primary hepatocytes were treated with 8 μM FINO2 for 3 h, Fe 2+ levels and lipid peroxidation were visualized using FerroOrange and C11-BODIPY staining respectively. Scale bar, 100 µm. F The schema illustrates HepG2 cells with ORM2 knockdown, cells were treated with FINO2 or RSL3, with cell survival, cell death, ferrous iron, and lipid peroxidation levels measured. G HepG2 cells with ORM2 knockdown were treated with FINO2 at the indicated concentrations for 12 h, and cell viability was assessed using CCK8. H HepG2 cells with ORM2 knockdown were treated with 8 μM FINO2 for 12 h, PI staining was measured. Quantification on the right. Scale bar, 100 μm. I – J HepG2 cells with ORM2 knockdown were treated with 8 μM FINO2 for 3 h, Fe 2+ levels and lipid peroxidation were visualized using FerroOrange and C11-BODIPY staining respectively. Scale bar, 100 μm. K Flag-ORM2 was overexpressed into HepG2 cells, cells were treated with FINO2 at indicated doses for 12 h. Cell viability was assessed using CCK8. L HepG2 cells with ORM2 overexpressing were treated with 8 μM FINO2 for 12 h, PI staining was measured. Quantification on the right. Scale bar, 100 μm. M – N HepG2 cells with ORM2 overexpressing were treated with 8 μM FINO2 for 3 h, Fe 2+ levels and lipid peroxidation were visualized using FerroOrange and C11-BODIPY staining, respectively. Scale bar, 100 μm. All data in this figure are represented as mean ± SEM. Data were analyzed by two-way ANOVA followed by Bonferroni’s multiple comparisons test for comparisons between genotypes. Exact p values are provided in the figure. All experiments were performed in triplicates.
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A The schema illustrates primary hepatocytes isolated from WT and Orm2 -/- mice, then treated with FINO2 or RSL3, with cell survival, cell death, ferrous iron, and lipid peroxidation levels measured. B WT and Orm2 -/- primary hepatocytes were treated with indicated doses of FINO2 for 12 h, cell viability was measured using CCK8. C WT and Orm2 -/- primary hepatocytes were treated with 8 μM FINO2 for 12 h, and <t>propidium</t> iodide (PI) staining to assess cell death. Quantification on the right. Scale bar, 100 μm. D – E WT and Orm2 -/- primary hepatocytes were treated with 8 μM FINO2 for 3 h, Fe 2+ levels and lipid peroxidation were visualized using FerroOrange and C11-BODIPY staining respectively. Scale bar, 100 µm. F The schema illustrates HepG2 cells with ORM2 knockdown, cells were treated with FINO2 or RSL3, with cell survival, cell death, ferrous iron, and lipid peroxidation levels measured. G HepG2 cells with ORM2 knockdown were treated with FINO2 at the indicated concentrations for 12 h, and cell viability was assessed using CCK8. H HepG2 cells with ORM2 knockdown were treated with 8 μM FINO2 for 12 h, PI staining was measured. Quantification on the right. Scale bar, 100 μm. I – J HepG2 cells with ORM2 knockdown were treated with 8 μM FINO2 for 3 h, Fe 2+ levels and lipid peroxidation were visualized using FerroOrange and C11-BODIPY staining respectively. Scale bar, 100 μm. K Flag-ORM2 was overexpressed into HepG2 cells, cells were treated with FINO2 at indicated doses for 12 h. Cell viability was assessed using CCK8. L HepG2 cells with ORM2 overexpressing were treated with 8 μM FINO2 for 12 h, PI staining was measured. Quantification on the right. Scale bar, 100 μm. M – N HepG2 cells with ORM2 overexpressing were treated with 8 μM FINO2 for 3 h, Fe 2+ levels and lipid peroxidation were visualized using FerroOrange and C11-BODIPY staining, respectively. Scale bar, 100 μm. All data in this figure are represented as mean ± SEM. Data were analyzed by two-way ANOVA followed by Bonferroni’s multiple comparisons test for comparisons between genotypes. Exact p values are provided in the figure. All experiments were performed in triplicates.
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BS combined with DAC showed enhanced effects in inhibiting the survival of lung cancer cells. A549 and H1299 cells were treated with BS, DAC, or BS + DAC (3:1 for A549 [BS-5 μM, DAC-1.67 μM] and 2:1 for H1299 [BS-5 μM, DAC-2.5 μM]) for 48 h, followed by <t>Annexin</t> V-PI staining. The results of total apoptosis (including both early and late apoptotic populations) are shown as mean ± SD. * P < 0.05, *** P < 0.001, **** P < 0.0001, compared with each indicated group by one-way ANOVA followed by Tukey’s post hoc test analysis ( n = 3).
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Image Search Results


A The schema illustrates primary hepatocytes isolated from WT and Orm2 -/- mice, then treated with FINO2 or RSL3, with cell survival, cell death, ferrous iron, and lipid peroxidation levels measured. B WT and Orm2 -/- primary hepatocytes were treated with indicated doses of FINO2 for 12 h, cell viability was measured using CCK8. C WT and Orm2 -/- primary hepatocytes were treated with 8 μM FINO2 for 12 h, and propidium iodide (PI) staining to assess cell death. Quantification on the right. Scale bar, 100 μm. D – E WT and Orm2 -/- primary hepatocytes were treated with 8 μM FINO2 for 3 h, Fe 2+ levels and lipid peroxidation were visualized using FerroOrange and C11-BODIPY staining respectively. Scale bar, 100 µm. F The schema illustrates HepG2 cells with ORM2 knockdown, cells were treated with FINO2 or RSL3, with cell survival, cell death, ferrous iron, and lipid peroxidation levels measured. G HepG2 cells with ORM2 knockdown were treated with FINO2 at the indicated concentrations for 12 h, and cell viability was assessed using CCK8. H HepG2 cells with ORM2 knockdown were treated with 8 μM FINO2 for 12 h, PI staining was measured. Quantification on the right. Scale bar, 100 μm. I – J HepG2 cells with ORM2 knockdown were treated with 8 μM FINO2 for 3 h, Fe 2+ levels and lipid peroxidation were visualized using FerroOrange and C11-BODIPY staining respectively. Scale bar, 100 μm. K Flag-ORM2 was overexpressed into HepG2 cells, cells were treated with FINO2 at indicated doses for 12 h. Cell viability was assessed using CCK8. L HepG2 cells with ORM2 overexpressing were treated with 8 μM FINO2 for 12 h, PI staining was measured. Quantification on the right. Scale bar, 100 μm. M – N HepG2 cells with ORM2 overexpressing were treated with 8 μM FINO2 for 3 h, Fe 2+ levels and lipid peroxidation were visualized using FerroOrange and C11-BODIPY staining, respectively. Scale bar, 100 μm. All data in this figure are represented as mean ± SEM. Data were analyzed by two-way ANOVA followed by Bonferroni’s multiple comparisons test for comparisons between genotypes. Exact p values are provided in the figure. All experiments were performed in triplicates.

Journal: Cell Death & Disease

Article Title: Hepatokine ORM2 suppresses pathological ferritinophagy to prevent acute tissue injury

doi: 10.1038/s41419-026-08803-0

Figure Lengend Snippet: A The schema illustrates primary hepatocytes isolated from WT and Orm2 -/- mice, then treated with FINO2 or RSL3, with cell survival, cell death, ferrous iron, and lipid peroxidation levels measured. B WT and Orm2 -/- primary hepatocytes were treated with indicated doses of FINO2 for 12 h, cell viability was measured using CCK8. C WT and Orm2 -/- primary hepatocytes were treated with 8 μM FINO2 for 12 h, and propidium iodide (PI) staining to assess cell death. Quantification on the right. Scale bar, 100 μm. D – E WT and Orm2 -/- primary hepatocytes were treated with 8 μM FINO2 for 3 h, Fe 2+ levels and lipid peroxidation were visualized using FerroOrange and C11-BODIPY staining respectively. Scale bar, 100 µm. F The schema illustrates HepG2 cells with ORM2 knockdown, cells were treated with FINO2 or RSL3, with cell survival, cell death, ferrous iron, and lipid peroxidation levels measured. G HepG2 cells with ORM2 knockdown were treated with FINO2 at the indicated concentrations for 12 h, and cell viability was assessed using CCK8. H HepG2 cells with ORM2 knockdown were treated with 8 μM FINO2 for 12 h, PI staining was measured. Quantification on the right. Scale bar, 100 μm. I – J HepG2 cells with ORM2 knockdown were treated with 8 μM FINO2 for 3 h, Fe 2+ levels and lipid peroxidation were visualized using FerroOrange and C11-BODIPY staining respectively. Scale bar, 100 μm. K Flag-ORM2 was overexpressed into HepG2 cells, cells were treated with FINO2 at indicated doses for 12 h. Cell viability was assessed using CCK8. L HepG2 cells with ORM2 overexpressing were treated with 8 μM FINO2 for 12 h, PI staining was measured. Quantification on the right. Scale bar, 100 μm. M – N HepG2 cells with ORM2 overexpressing were treated with 8 μM FINO2 for 3 h, Fe 2+ levels and lipid peroxidation were visualized using FerroOrange and C11-BODIPY staining, respectively. Scale bar, 100 μm. All data in this figure are represented as mean ± SEM. Data were analyzed by two-way ANOVA followed by Bonferroni’s multiple comparisons test for comparisons between genotypes. Exact p values are provided in the figure. All experiments were performed in triplicates.

Article Snippet: Cell death was assessed using propidium iodide (PI) staining (LianKe Bio, AP107-30).

Techniques: Isolation, Staining, Knockdown

BS combined with DAC showed enhanced effects in inhibiting the survival of lung cancer cells. A549 and H1299 cells were treated with BS, DAC, or BS + DAC (3:1 for A549 [BS-5 μM, DAC-1.67 μM] and 2:1 for H1299 [BS-5 μM, DAC-2.5 μM]) for 48 h, followed by Annexin V-PI staining. The results of total apoptosis (including both early and late apoptotic populations) are shown as mean ± SD. * P < 0.05, *** P < 0.001, **** P < 0.0001, compared with each indicated group by one-way ANOVA followed by Tukey’s post hoc test analysis ( n = 3).

Journal: Scientific Reports

Article Title: The combined inhibitory effect of butaselen and decitabine against lung cancer cells

doi: 10.1038/s41598-026-45054-7

Figure Lengend Snippet: BS combined with DAC showed enhanced effects in inhibiting the survival of lung cancer cells. A549 and H1299 cells were treated with BS, DAC, or BS + DAC (3:1 for A549 [BS-5 μM, DAC-1.67 μM] and 2:1 for H1299 [BS-5 μM, DAC-2.5 μM]) for 48 h, followed by Annexin V-PI staining. The results of total apoptosis (including both early and late apoptotic populations) are shown as mean ± SD. * P < 0.05, *** P < 0.001, **** P < 0.0001, compared with each indicated group by one-way ANOVA followed by Tukey’s post hoc test analysis ( n = 3).

Article Snippet: The cells were collected, and the apoptosis assay was conducted using the Annexin V-FITC/ propidium iodide (PI) Dual Staining Kit (KeyGEN) as instructed by the manufacturer and described previously .

Techniques: Staining