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MedChemExpress human orm2 protein
<t>Orm2</t> expression in livers of wild-type (WT) mice at different times following 300 mg/kg APAP treatment, measured by qPCR ( A ) ( n = 3 (0 h), n = 5 (6 h), n = 4 (12 h and 24 h)) and western blot ( B ) ( n = 4 per group). Vinculin (VINC) was used as the loading control. C Representative gross liver and H&E images from WT and Orm2 -/- mice at 24 h post-APAP. Scale bar, 200 μm. Necrotic areas circled in white lines, with quantification of necrosis and areas of patchy hemorrhages shown below ( n = 4 per group). D Serum levels of ALT and AST in WT and Orm2 -/- mice at 24 h post-APAP. E Apoptosis measured by TUNEL staining from WT and Orm2 -/- mice at 24 h post-APAP. Scale bar, 200 μm. Quantification is on the right. F Survival curves of WT and Orm2 -/- mice treated with a lethal dose of APAP (750 mg/kg) ( n = 10 per group). Eight-week-old WT male mice were injected retro-orbitally with Ad- ORM2 or Ad- vector virus. After two weeks, WT and Orm2 -/- mice received 300 mg/kg APAP intraperitoneally. 24 h later, ORM2 protein and mRNA levels in liver tissue ( G ), liver morphology ( H ), H&E ( H ), serum ALT and AST levels ( I ), as well as TUNEL staining ( J ), were assessed ( n = 5 per group). Scale bars, 100 μm. All data are presented as mean ± SEM. In ( A ), data were analyzed by one-way ANOVA with Dunnett’s test. In ( F ), the survival curve was compared using the log-rank (Mantel–Cox) test, and the remaining data were analyzed by unpaired two-tailed Student’s t test. Exact p values are provided in the figure, *** p < 0.001, **** p < 0.0001. “n” refers to biological replicates. All experiments were performed in triplicates.
Human Orm2 Protein, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Sino Biological orm2
Multiplex SERS detection of ANXA11, <t>ORM2,</t> SERPINA3, and ATRN in serum samples from MPP⁺ (P1‐P13) and MPP⁻ (P14‐P22) LUAD patients. A) SERS signatures of individual patients, with error bars representing the SEM from three independent experiments. Comparison of average expression levels of B) ANXA11, C) ORM2, D) SERPINA3, and E) ATRN between MPP⁺ and MPP⁻ LUAD patients. Statistical significance was assessed using the unpaired two‐tailed t‐test. * P < 0.05; ** P < 0.01.
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Thermo Fisher gene exp orm2 mm04213463 g1

Gene Exp Orm2 Mm04213463 G1, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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MedChemExpress orm2
Reduced pancreatic <t>ORM2</t> expression in AP. (A) Scatterplots showing log2 transformation of the normalized blood ORM1 in patients with MAP (n=57) and healthy controls (n=32). (B) Scatterplots showing log2 transformation of the normalized blood ORM2 in patients with MAP (n=57) and healthy controls (n=32). (C) The serum ORM in control and AP mice (n=6 per group). (D) Immunoblotting of ORM1 and ORM2 in serum from control and AP mice (n=6 per group). (E) Immunoblotting and quantitative analysis of ORM1 and ORM2 in pancreas from control and AP mice (n=6 per group). (F) Immunoblotting and quantitative analysis of ORM1 and ORM2 in liver from control and AP mice (n=6 per group). Data are presented as mean ± SEM. The groups were compared using unpaired two-tailed student’s t -test (*, P<0.05; ***, P<0.001; ****, P<0.0001). AP, acute pancreatitis; MAP, mild acute pancreatitis; ORM, orosomucoid; SEM, standard error of the mean.
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Biorbyt human orm2
Reduced pancreatic <t>ORM2</t> expression in AP. (A) Scatterplots showing log2 transformation of the normalized blood ORM1 in patients with MAP (n=57) and healthy controls (n=32). (B) Scatterplots showing log2 transformation of the normalized blood ORM2 in patients with MAP (n=57) and healthy controls (n=32). (C) The serum ORM in control and AP mice (n=6 per group). (D) Immunoblotting of ORM1 and ORM2 in serum from control and AP mice (n=6 per group). (E) Immunoblotting and quantitative analysis of ORM1 and ORM2 in pancreas from control and AP mice (n=6 per group). (F) Immunoblotting and quantitative analysis of ORM1 and ORM2 in liver from control and AP mice (n=6 per group). Data are presented as mean ± SEM. The groups were compared using unpaired two-tailed student’s t -test (*, P<0.05; ***, P<0.001; ****, P<0.0001). AP, acute pancreatitis; MAP, mild acute pancreatitis; ORM, orosomucoid; SEM, standard error of the mean.
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OriGene orm2
Reduced pancreatic <t>ORM2</t> expression in AP. (A) Scatterplots showing log2 transformation of the normalized blood ORM1 in patients with MAP (n=57) and healthy controls (n=32). (B) Scatterplots showing log2 transformation of the normalized blood ORM2 in patients with MAP (n=57) and healthy controls (n=32). (C) The serum ORM in control and AP mice (n=6 per group). (D) Immunoblotting of ORM1 and ORM2 in serum from control and AP mice (n=6 per group). (E) Immunoblotting and quantitative analysis of ORM1 and ORM2 in pancreas from control and AP mice (n=6 per group). (F) Immunoblotting and quantitative analysis of ORM1 and ORM2 in liver from control and AP mice (n=6 per group). Data are presented as mean ± SEM. The groups were compared using unpaired two-tailed student’s t -test (*, P<0.05; ***, P<0.001; ****, P<0.0001). AP, acute pancreatitis; MAP, mild acute pancreatitis; ORM, orosomucoid; SEM, standard error of the mean.
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Shanghai GenePharma orm2 sirna
Reduced pancreatic <t>ORM2</t> expression in AP. (A) Scatterplots showing log2 transformation of the normalized blood ORM1 in patients with MAP (n=57) and healthy controls (n=32). (B) Scatterplots showing log2 transformation of the normalized blood ORM2 in patients with MAP (n=57) and healthy controls (n=32). (C) The serum ORM in control and AP mice (n=6 per group). (D) Immunoblotting of ORM1 and ORM2 in serum from control and AP mice (n=6 per group). (E) Immunoblotting and quantitative analysis of ORM1 and ORM2 in pancreas from control and AP mice (n=6 per group). (F) Immunoblotting and quantitative analysis of ORM1 and ORM2 in liver from control and AP mice (n=6 per group). Data are presented as mean ± SEM. The groups were compared using unpaired two-tailed student’s t -test (*, P<0.05; ***, P<0.001; ****, P<0.0001). AP, acute pancreatitis; MAP, mild acute pancreatitis; ORM, orosomucoid; SEM, standard error of the mean.
Orm2 Sirna, supplied by Shanghai GenePharma, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Image Search Results


Orm2 expression in livers of wild-type (WT) mice at different times following 300 mg/kg APAP treatment, measured by qPCR ( A ) ( n = 3 (0 h), n = 5 (6 h), n = 4 (12 h and 24 h)) and western blot ( B ) ( n = 4 per group). Vinculin (VINC) was used as the loading control. C Representative gross liver and H&E images from WT and Orm2 -/- mice at 24 h post-APAP. Scale bar, 200 μm. Necrotic areas circled in white lines, with quantification of necrosis and areas of patchy hemorrhages shown below ( n = 4 per group). D Serum levels of ALT and AST in WT and Orm2 -/- mice at 24 h post-APAP. E Apoptosis measured by TUNEL staining from WT and Orm2 -/- mice at 24 h post-APAP. Scale bar, 200 μm. Quantification is on the right. F Survival curves of WT and Orm2 -/- mice treated with a lethal dose of APAP (750 mg/kg) ( n = 10 per group). Eight-week-old WT male mice were injected retro-orbitally with Ad- ORM2 or Ad- vector virus. After two weeks, WT and Orm2 -/- mice received 300 mg/kg APAP intraperitoneally. 24 h later, ORM2 protein and mRNA levels in liver tissue ( G ), liver morphology ( H ), H&E ( H ), serum ALT and AST levels ( I ), as well as TUNEL staining ( J ), were assessed ( n = 5 per group). Scale bars, 100 μm. All data are presented as mean ± SEM. In ( A ), data were analyzed by one-way ANOVA with Dunnett’s test. In ( F ), the survival curve was compared using the log-rank (Mantel–Cox) test, and the remaining data were analyzed by unpaired two-tailed Student’s t test. Exact p values are provided in the figure, *** p < 0.001, **** p < 0.0001. “n” refers to biological replicates. 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: Orm2 expression in livers of wild-type (WT) mice at different times following 300 mg/kg APAP treatment, measured by qPCR ( A ) ( n = 3 (0 h), n = 5 (6 h), n = 4 (12 h and 24 h)) and western blot ( B ) ( n = 4 per group). Vinculin (VINC) was used as the loading control. C Representative gross liver and H&E images from WT and Orm2 -/- mice at 24 h post-APAP. Scale bar, 200 μm. Necrotic areas circled in white lines, with quantification of necrosis and areas of patchy hemorrhages shown below ( n = 4 per group). D Serum levels of ALT and AST in WT and Orm2 -/- mice at 24 h post-APAP. E Apoptosis measured by TUNEL staining from WT and Orm2 -/- mice at 24 h post-APAP. Scale bar, 200 μm. Quantification is on the right. F Survival curves of WT and Orm2 -/- mice treated with a lethal dose of APAP (750 mg/kg) ( n = 10 per group). Eight-week-old WT male mice were injected retro-orbitally with Ad- ORM2 or Ad- vector virus. After two weeks, WT and Orm2 -/- mice received 300 mg/kg APAP intraperitoneally. 24 h later, ORM2 protein and mRNA levels in liver tissue ( G ), liver morphology ( H ), H&E ( H ), serum ALT and AST levels ( I ), as well as TUNEL staining ( J ), were assessed ( n = 5 per group). Scale bars, 100 μm. All data are presented as mean ± SEM. In ( A ), data were analyzed by one-way ANOVA with Dunnett’s test. In ( F ), the survival curve was compared using the log-rank (Mantel–Cox) test, and the remaining data were analyzed by unpaired two-tailed Student’s t test. Exact p values are provided in the figure, *** p < 0.001, **** p < 0.0001. “n” refers to biological replicates. All experiments were performed in triplicates.

Article Snippet: Human ORM2 protein (MedChem Express, HY-P7490).

Techniques: Expressing, Western Blot, Control, TUNEL Assay, Staining, Injection, Plasmid Preparation, Virus, Two Tailed Test

A Differentially enriched gene pathways from RNA-seq analysis of liver tissues in Orm2 -/- versus WT mice 24 h after APAP treatment ( n = 3 per group). B WT and Orm2 -/- mice were injected intraperitoneally with APAP (300 mg/kg). Liver samples were collected at the indicated time points for frozen section preparation. Sections were stained with FerroOrange to detect ferrous iron, with DAPI counterstaining. Mean FerroOrange fluorescence intensity is quantified below ( n = 3 per group, except 24 h: n = 4). Scale bars, 50 μm. C WT and Orm2 -/- mice were received APAP (300 mg/kg). Liver samples were collected at the indicated time points for frozen section preparation. Representative immunohistochemical staining for 4-HNE in liver sections, with mean intensity is quantified below ( n = 3 per group). Scale bars, 100 μm. D Measurement of malondialdehyde (MDA) levels in liver tissue from ( C ) ( n = 3 per group). E WT and Orm2 -/- mice were pre-treated with 200 mg/kg DFO or vehicle 2 h before APAP injection, with samples collected 24 h post-APAP. Representative H&E images of liver sections from mice, white dashed lines indicating cell death areas ( n = 4 per group). Scale bar, 100 μm. Damage areas were quantified on the right. F Serum ALT levels from mice in ( E ) were measured. G Primary hepatocytes isolated from WT and Orm2 -/- mice were treated with indicated concentrations of APAP and cell viability was measured using Cell Counting Kit 8 (CCK8). H Primary hepatocytes from WT and Orm2 -/- mice were treated with 5 μM APAP for the indicated times. LPO levels were measured. I Primary hepatocytes isolated from WT and Orm2 -/- mice were treated with 5 μM APAP in the presence of Fer-1 (2 μM) or DFO (50 μM), and cell viability was measured using CCK8. 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, and by one-way ANOVA with Dunnett’s test or unpaired t-test for comparisons between two or multiple experimental groups within the same genotype, respectively. Exact p values are provided in the figure, * p < 0.05, **** p < 0.0001, ns (no significance). 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 Differentially enriched gene pathways from RNA-seq analysis of liver tissues in Orm2 -/- versus WT mice 24 h after APAP treatment ( n = 3 per group). B WT and Orm2 -/- mice were injected intraperitoneally with APAP (300 mg/kg). Liver samples were collected at the indicated time points for frozen section preparation. Sections were stained with FerroOrange to detect ferrous iron, with DAPI counterstaining. Mean FerroOrange fluorescence intensity is quantified below ( n = 3 per group, except 24 h: n = 4). Scale bars, 50 μm. C WT and Orm2 -/- mice were received APAP (300 mg/kg). Liver samples were collected at the indicated time points for frozen section preparation. Representative immunohistochemical staining for 4-HNE in liver sections, with mean intensity is quantified below ( n = 3 per group). Scale bars, 100 μm. D Measurement of malondialdehyde (MDA) levels in liver tissue from ( C ) ( n = 3 per group). E WT and Orm2 -/- mice were pre-treated with 200 mg/kg DFO or vehicle 2 h before APAP injection, with samples collected 24 h post-APAP. Representative H&E images of liver sections from mice, white dashed lines indicating cell death areas ( n = 4 per group). Scale bar, 100 μm. Damage areas were quantified on the right. F Serum ALT levels from mice in ( E ) were measured. G Primary hepatocytes isolated from WT and Orm2 -/- mice were treated with indicated concentrations of APAP and cell viability was measured using Cell Counting Kit 8 (CCK8). H Primary hepatocytes from WT and Orm2 -/- mice were treated with 5 μM APAP for the indicated times. LPO levels were measured. I Primary hepatocytes isolated from WT and Orm2 -/- mice were treated with 5 μM APAP in the presence of Fer-1 (2 μM) or DFO (50 μM), and cell viability was measured using CCK8. 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, and by one-way ANOVA with Dunnett’s test or unpaired t-test for comparisons between two or multiple experimental groups within the same genotype, respectively. Exact p values are provided in the figure, * p < 0.05, **** p < 0.0001, ns (no significance). All experiments were performed in triplicates.

Article Snippet: Human ORM2 protein (MedChem Express, HY-P7490).

Techniques: RNA Sequencing, Injection, Staining, Fluorescence, Immunohistochemical staining, Isolation, Cell Counting

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: Human ORM2 protein (MedChem Express, HY-P7490).

Techniques: Isolation, Staining, Knockdown

A HepG2 cells with shNC or sh ORM2 knockdown were treated with 8 μM FINO2 for the indicated time points, western blot to detect FTH1 and ORM2 protein expression. B HepG2 cells with shNC or sh ORM2 knockdown were treated with 8 μM FINO2 for 6 h. The intracellular ferrous ion (Fe 2+ ) levels were stained with FerroOrange (0.25 µmol/L) and analyzed by flow cytometry. C Primary hepatocytes were isolated from WT and Orm2 -/- mice, and cells were treated with 8 μM FINO2 and 10 μM Chloroquine (CQ). FTH1 protein expression was measured by western blot. D HepG2 cells with ORM2 knockdown or control were treated with 8 μM FINO2. Representative immunofluorescence images display ferritin (FTL) and lysosomes (LAMP2 positive foci) localization. Quantification of co-localization was analyzed using Image J (right panel). Scale bars, 5 μm. E WT and Orm2 -/- mice were injected with APAP. 24 h post-APAP, liver tissues were collected and lysed for FTL co-immunoprecipitation (co-IP), and TAX1BP1, NCOA4, FTL, and GAPDH antibodies were used for IB. F HEK293T cells were co-transfected with Flag-ORM2 and Myc-NCOA4 plasmids. Cells were treated with 8 μM FINO2 or vehicle for 3 h, followed by co-IP using Myc beads. Flag-ORM2 levels in the co-IP complexes were analyzed. G HEK293T cells were co-transfected with Flag-TAX1BP1 and HA-ORM2 . Cells were treated with 8 μM FINO2 or vehicle for 3 h, followed by co-IP using Flag beads. HA-ORM2 protein were measured. H HepG2 cells were overexpressed with Flag-ORM2 plasmid. Cells were treated with 4 μM RSL3. Representative immunofluorescence images of TAX1BP1 and FTL were detected, and the Pearson correlation for co-localization was quantified using ImageJ. Scale bars, 5 μm. I HEK293T cells were co-transfected with Flag-TAX1BP1 , Myc-NCOA4 , and increasing amounts of HA-ORM2 plasmids. Cells were then treated with 8 μM FINO2 plus 10 μM chloroquine (CQ) or DMSO vehicle. Co-IP were performed using Myc beads, and Flag, HA, Myc, and GAPDH antibodies were used for IB. J A model illustrates that ORM2 inhibits ferritin localization to lysosomes during ferroptosis by modulating NCOA4-TAX1BP1 interactions, reducing intracellular ferrous ions. All data in this figure are represented as mean ± SEM. In ( B ), data were analyzed by two-way ANOVA followed by Bonferroni’s multiple comparisons test; in ( D ) and ( H ), by unpaired t -test. 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 HepG2 cells with shNC or sh ORM2 knockdown were treated with 8 μM FINO2 for the indicated time points, western blot to detect FTH1 and ORM2 protein expression. B HepG2 cells with shNC or sh ORM2 knockdown were treated with 8 μM FINO2 for 6 h. The intracellular ferrous ion (Fe 2+ ) levels were stained with FerroOrange (0.25 µmol/L) and analyzed by flow cytometry. C Primary hepatocytes were isolated from WT and Orm2 -/- mice, and cells were treated with 8 μM FINO2 and 10 μM Chloroquine (CQ). FTH1 protein expression was measured by western blot. D HepG2 cells with ORM2 knockdown or control were treated with 8 μM FINO2. Representative immunofluorescence images display ferritin (FTL) and lysosomes (LAMP2 positive foci) localization. Quantification of co-localization was analyzed using Image J (right panel). Scale bars, 5 μm. E WT and Orm2 -/- mice were injected with APAP. 24 h post-APAP, liver tissues were collected and lysed for FTL co-immunoprecipitation (co-IP), and TAX1BP1, NCOA4, FTL, and GAPDH antibodies were used for IB. F HEK293T cells were co-transfected with Flag-ORM2 and Myc-NCOA4 plasmids. Cells were treated with 8 μM FINO2 or vehicle for 3 h, followed by co-IP using Myc beads. Flag-ORM2 levels in the co-IP complexes were analyzed. G HEK293T cells were co-transfected with Flag-TAX1BP1 and HA-ORM2 . Cells were treated with 8 μM FINO2 or vehicle for 3 h, followed by co-IP using Flag beads. HA-ORM2 protein were measured. H HepG2 cells were overexpressed with Flag-ORM2 plasmid. Cells were treated with 4 μM RSL3. Representative immunofluorescence images of TAX1BP1 and FTL were detected, and the Pearson correlation for co-localization was quantified using ImageJ. Scale bars, 5 μm. I HEK293T cells were co-transfected with Flag-TAX1BP1 , Myc-NCOA4 , and increasing amounts of HA-ORM2 plasmids. Cells were then treated with 8 μM FINO2 plus 10 μM chloroquine (CQ) or DMSO vehicle. Co-IP were performed using Myc beads, and Flag, HA, Myc, and GAPDH antibodies were used for IB. J A model illustrates that ORM2 inhibits ferritin localization to lysosomes during ferroptosis by modulating NCOA4-TAX1BP1 interactions, reducing intracellular ferrous ions. All data in this figure are represented as mean ± SEM. In ( B ), data were analyzed by two-way ANOVA followed by Bonferroni’s multiple comparisons test; in ( D ) and ( H ), by unpaired t -test. Exact p values are provided in the figure. All experiments were performed in triplicates.

Article Snippet: Human ORM2 protein (MedChem Express, HY-P7490).

Techniques: Knockdown, Western Blot, Expressing, Staining, Flow Cytometry, Isolation, Control, Immunofluorescence, Injection, Immunoprecipitation, Co-Immunoprecipitation Assay, Transfection, Plasmid Preparation

A WT mice were pre-injected intraperitoneally with recombinant ORM2 protein (rORM2, 7 mg/kg) or PBS for 2 h, followed by 300 mg/kg APAP. After 24 h, liver samples were collected for ORM2 expression analysis by western blot ( n = 4 and 3). B Representative liver morphology and H&E images of livers from mice in ( A ). Scale bar, 200 μm. C – F Serum ALT, AST, LPO, liver FTH1 protein and liver iron levels were measured from mice in ( A ), ( n = 4-3 per group). G WT mice received 7 mg/kg rORM2 or PBS 2 h before 750 mg/kg APAP, and survival curves were plotted, ( n = 12 per group). H WT mice were injected intraperitoneally with APAP (250 mg/kg) to induce liver injury. At 1.5- and 12-h post-APAP injection, mice received equal volumes of PBS, rORM2 (20 mg/kg), or NAC (300 mg/kg) as indicated. Serum samples were collected at 24 h after APAP, serum ALT and AST were measured ( n = 3 per group). I Representative H&E staining of liver sections from the indicated groups in ( H ). Scale bar, 100 μm. J WT mice received 7 mg/kg rORM2 2 h before performing liver ischemia-reperfusion (HIR). 12 h post-HIR, livers were collected for H&E, the white dashed lines indicated the damaged area ( n = 3 per group). Scale bar, 100 μm. K – L Serum ALT, AST, liver iron content, and liver MDA from mice in ( J ) were measured, ( n = 3 per group). All data in this figure are represented as mean ± SEM. In ( G ), the survival curve was compared using the log-rank (Mantel-Cox) test; In ( H ) data were analyzed by two-way ANOVA followed by Bonferroni’s multiple comparisons test for comparisons between rORM2 and NAC groups, and by one-way ANOVA with Dunnett’s test for comparisons between APAP + PBS and rORM2+APAP groups; the remaining data were analyzed by unpaired two-tailed Student’s t test. Exact p values are provided in the figure. “n” refers to biological replicates. 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 WT mice were pre-injected intraperitoneally with recombinant ORM2 protein (rORM2, 7 mg/kg) or PBS for 2 h, followed by 300 mg/kg APAP. After 24 h, liver samples were collected for ORM2 expression analysis by western blot ( n = 4 and 3). B Representative liver morphology and H&E images of livers from mice in ( A ). Scale bar, 200 μm. C – F Serum ALT, AST, LPO, liver FTH1 protein and liver iron levels were measured from mice in ( A ), ( n = 4-3 per group). G WT mice received 7 mg/kg rORM2 or PBS 2 h before 750 mg/kg APAP, and survival curves were plotted, ( n = 12 per group). H WT mice were injected intraperitoneally with APAP (250 mg/kg) to induce liver injury. At 1.5- and 12-h post-APAP injection, mice received equal volumes of PBS, rORM2 (20 mg/kg), or NAC (300 mg/kg) as indicated. Serum samples were collected at 24 h after APAP, serum ALT and AST were measured ( n = 3 per group). I Representative H&E staining of liver sections from the indicated groups in ( H ). Scale bar, 100 μm. J WT mice received 7 mg/kg rORM2 2 h before performing liver ischemia-reperfusion (HIR). 12 h post-HIR, livers were collected for H&E, the white dashed lines indicated the damaged area ( n = 3 per group). Scale bar, 100 μm. K – L Serum ALT, AST, liver iron content, and liver MDA from mice in ( J ) were measured, ( n = 3 per group). All data in this figure are represented as mean ± SEM. In ( G ), the survival curve was compared using the log-rank (Mantel-Cox) test; In ( H ) data were analyzed by two-way ANOVA followed by Bonferroni’s multiple comparisons test for comparisons between rORM2 and NAC groups, and by one-way ANOVA with Dunnett’s test for comparisons between APAP + PBS and rORM2+APAP groups; the remaining data were analyzed by unpaired two-tailed Student’s t test. Exact p values are provided in the figure. “n” refers to biological replicates. All experiments were performed in triplicates.

Article Snippet: Human ORM2 protein (MedChem Express, HY-P7490).

Techniques: Injection, Recombinant, Expressing, Western Blot, Staining, Two Tailed Test

A Wild-type mice underwent sham or renal ischemia-reperfusion (KIR) surgery. Serum samples were collected at 12 h. ORM2 protein level of the serum was quantified relative to total protein using Ponceau S staining and western blot ( n = 4 per group). B Kidney ORM2 protein levels; liver and kidney Orm2 mRNA from ( A ) were measured by western blot and qPCR. C Wild-type mice underwent sham or renal ischemia-reperfusion (KIR) surgery, kidney samples were collected for H&E and ORM2 staining. H&E staining shows swelling (*) and nuclear condensation (→) of renal tubular epithelial cells ( n = 3 per group). Scale bars, 100 μm. D Sleeping beauty transposon PT3-Vector or PT3- Orm2-EGFP and SB100 transposase were delivered via hydrodynamic tail vein injection (HDT) in mice. One week later, mice underwent either sham or KIR surgery. EGFP-ORM2 expression in kidney sections was assessed by immunohistochemistry ( n = 3 per group). Scale bars, 50 μm. E WT and Orm2 -/- mice underwent KIR surgery, kidney samples were collected 12 h post-surgery. H&E staining shows swelling (*) and nuclear condensation (→) of renal tubular epithelial cells ( n = 3 (WT mice), n = 4 ( Orm2 -/- mice)). Scale bars, 100 μm. F Serum creatinine and blood urea nitrogen (BUN) levels of mice in ( E ) were measured 12 h post-KIR. G Lipid peroxidation (LPO) in kidney tissues of mice in ( E ) ( n = 3 per group). H WT and Orm2 -/- mice underwent intestinal ischemia-reperfusion (IIR) surgery, lung samples were collected 3 h post-surgery. Images show H&E staining of lung sections ( n = 3 per group). Scale bars, 50 μm. I Malondialdehyde (MDA) levels of lung samples from mice in ( H ) ( n = 3 per group). All data in this figure are represented as mean ± SEM. In ( I ), data were analyzed by two-way ANOVA followed by Bonferroni’s multiple comparisons test; the remaining data were analyzed by unpaired two-tailed Student’s t test. Exact p values are provided in the figure. “n” refers to biological replicates. 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 Wild-type mice underwent sham or renal ischemia-reperfusion (KIR) surgery. Serum samples were collected at 12 h. ORM2 protein level of the serum was quantified relative to total protein using Ponceau S staining and western blot ( n = 4 per group). B Kidney ORM2 protein levels; liver and kidney Orm2 mRNA from ( A ) were measured by western blot and qPCR. C Wild-type mice underwent sham or renal ischemia-reperfusion (KIR) surgery, kidney samples were collected for H&E and ORM2 staining. H&E staining shows swelling (*) and nuclear condensation (→) of renal tubular epithelial cells ( n = 3 per group). Scale bars, 100 μm. D Sleeping beauty transposon PT3-Vector or PT3- Orm2-EGFP and SB100 transposase were delivered via hydrodynamic tail vein injection (HDT) in mice. One week later, mice underwent either sham or KIR surgery. EGFP-ORM2 expression in kidney sections was assessed by immunohistochemistry ( n = 3 per group). Scale bars, 50 μm. E WT and Orm2 -/- mice underwent KIR surgery, kidney samples were collected 12 h post-surgery. H&E staining shows swelling (*) and nuclear condensation (→) of renal tubular epithelial cells ( n = 3 (WT mice), n = 4 ( Orm2 -/- mice)). Scale bars, 100 μm. F Serum creatinine and blood urea nitrogen (BUN) levels of mice in ( E ) were measured 12 h post-KIR. G Lipid peroxidation (LPO) in kidney tissues of mice in ( E ) ( n = 3 per group). H WT and Orm2 -/- mice underwent intestinal ischemia-reperfusion (IIR) surgery, lung samples were collected 3 h post-surgery. Images show H&E staining of lung sections ( n = 3 per group). Scale bars, 50 μm. I Malondialdehyde (MDA) levels of lung samples from mice in ( H ) ( n = 3 per group). All data in this figure are represented as mean ± SEM. In ( I ), data were analyzed by two-way ANOVA followed by Bonferroni’s multiple comparisons test; the remaining data were analyzed by unpaired two-tailed Student’s t test. Exact p values are provided in the figure. “n” refers to biological replicates. All experiments were performed in triplicates.

Article Snippet: Human ORM2 protein (MedChem Express, HY-P7490).

Techniques: Staining, Western Blot, Plasmid Preparation, Injection, Expressing, Immunohistochemistry, Two Tailed Test

A Wild-type mice received 7 mg/kg recombinant mouse ORM2-Fc protein (rORM2) 2 h before KIR. Kidney sections stained with H&E and Prussian blue. Scale bars, 100 μm. B Urine creatinine and blood urea nitrogen (BUN) levels at 12 h from mouse urine samples in ( A ) ( n = 3 per group). C Wild-type mice received 7 mg/kg rORM2 2 h before intestinal I/R (IIR), lung samples were collected at 3 h post-surgery and stained for H&E and ORM2 ( n = 4 per group). Scale bars, 50 μm. D Iron and MDA levels of lung samples from ( C ) are presented ( n = 4 per group). E HEK293T cells were incubated with 1 μg/mL rORM2 protein with or without 1 μM RSL3 treatment for 6 h. Images show rORM2 and LAMP1 localization. Scale bars, 5 μm. F Western blot analysis of rORM2 levels in HEK293T cells after an 8-h incubation with the indicated concentrations of ORM2 recombinant protein in the media. G HEK293T cells were pretreated with 1 μg/mL rORM2 proteins for 2 h, followed by 8 μM FINO2 for 6 h. FerroOrange staining was used to assess ferrous ion levels. Scale bars, 100 μm. H HEK293T cells were treated with Amiloride (2 μM) for 2 h, then incubated with or without 1 μg/mL rORM2 for 2 h. Cells were then exposed to 8 μM FINO2 for 12 h, and cell viability was measured using CCK8 assay. I A model suggests that ischemia-reperfusion injuries increase hepatic ORM2 production and secretion. Circulating or recombinant ORM2 protein then mitigates the injury by inhibiting ferroptosis. All data in this figure are represented as mean ± SEM. In ( H ), data were analyzed by two-way ANOVA followed by Bonferroni’s multiple comparisons test; the remaining data were analyzed by unpaired two-tailed Student’s t test. Exact p values are provided in the figure. “n” refers to biological replicates. 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 Wild-type mice received 7 mg/kg recombinant mouse ORM2-Fc protein (rORM2) 2 h before KIR. Kidney sections stained with H&E and Prussian blue. Scale bars, 100 μm. B Urine creatinine and blood urea nitrogen (BUN) levels at 12 h from mouse urine samples in ( A ) ( n = 3 per group). C Wild-type mice received 7 mg/kg rORM2 2 h before intestinal I/R (IIR), lung samples were collected at 3 h post-surgery and stained for H&E and ORM2 ( n = 4 per group). Scale bars, 50 μm. D Iron and MDA levels of lung samples from ( C ) are presented ( n = 4 per group). E HEK293T cells were incubated with 1 μg/mL rORM2 protein with or without 1 μM RSL3 treatment for 6 h. Images show rORM2 and LAMP1 localization. Scale bars, 5 μm. F Western blot analysis of rORM2 levels in HEK293T cells after an 8-h incubation with the indicated concentrations of ORM2 recombinant protein in the media. G HEK293T cells were pretreated with 1 μg/mL rORM2 proteins for 2 h, followed by 8 μM FINO2 for 6 h. FerroOrange staining was used to assess ferrous ion levels. Scale bars, 100 μm. H HEK293T cells were treated with Amiloride (2 μM) for 2 h, then incubated with or without 1 μg/mL rORM2 for 2 h. Cells were then exposed to 8 μM FINO2 for 12 h, and cell viability was measured using CCK8 assay. I A model suggests that ischemia-reperfusion injuries increase hepatic ORM2 production and secretion. Circulating or recombinant ORM2 protein then mitigates the injury by inhibiting ferroptosis. All data in this figure are represented as mean ± SEM. In ( H ), data were analyzed by two-way ANOVA followed by Bonferroni’s multiple comparisons test; the remaining data were analyzed by unpaired two-tailed Student’s t test. Exact p values are provided in the figure. “n” refers to biological replicates. All experiments were performed in triplicates.

Article Snippet: Human ORM2 protein (MedChem Express, HY-P7490).

Techniques: Recombinant, Staining, Incubation, Western Blot, CCK-8 Assay, Two Tailed Test

Multiplex SERS detection of ANXA11, ORM2, SERPINA3, and ATRN in serum samples from MPP⁺ (P1‐P13) and MPP⁻ (P14‐P22) LUAD patients. A) SERS signatures of individual patients, with error bars representing the SEM from three independent experiments. Comparison of average expression levels of B) ANXA11, C) ORM2, D) SERPINA3, and E) ATRN between MPP⁺ and MPP⁻ LUAD patients. Statistical significance was assessed using the unpaired two‐tailed t‐test. * P < 0.05; ** P < 0.01.

Journal: Advanced Science

Article Title: Proteomics‐Empowered Microfluidic‐SERS Immunoassay for Identifying and Detecting Biomarkers of Micropapillary Lung Adenocarcinoma

doi: 10.1002/advs.202501336

Figure Lengend Snippet: Multiplex SERS detection of ANXA11, ORM2, SERPINA3, and ATRN in serum samples from MPP⁺ (P1‐P13) and MPP⁻ (P14‐P22) LUAD patients. A) SERS signatures of individual patients, with error bars representing the SEM from three independent experiments. Comparison of average expression levels of B) ANXA11, C) ORM2, D) SERPINA3, and E) ATRN between MPP⁺ and MPP⁻ LUAD patients. Statistical significance was assessed using the unpaired two‐tailed t‐test. * P < 0.05; ** P < 0.01.

Article Snippet: Antibodies against ATRN (Cat.: 202440‐T02), ORM2 (Cat.: 13299‐T16), SERPINA3 (Cat.: 10307‐RP02), and recombinant protein A (Cat.: 10600‐P07E) were acquired from Sino Biological.

Techniques: Multiplex Assay, Comparison, Expressing, Two Tailed Test

Machine learning models based on SERS signatures of serum ANXA11, ORM2, SERPINA3, and ATRN for differentiating MPP⁺ (P1‐P13) and MPP⁻ (P14‐P22) LUAD patients. A) Random Forest, B) Logistic Regression, C) Naive Bayes, D) Decision Tree, E) Hierarchical Clustering, F) k‐Means, G) Louvain Clustering, H) DBSCAN, and I) their corresponding AUCs.

Journal: Advanced Science

Article Title: Proteomics‐Empowered Microfluidic‐SERS Immunoassay for Identifying and Detecting Biomarkers of Micropapillary Lung Adenocarcinoma

doi: 10.1002/advs.202501336

Figure Lengend Snippet: Machine learning models based on SERS signatures of serum ANXA11, ORM2, SERPINA3, and ATRN for differentiating MPP⁺ (P1‐P13) and MPP⁻ (P14‐P22) LUAD patients. A) Random Forest, B) Logistic Regression, C) Naive Bayes, D) Decision Tree, E) Hierarchical Clustering, F) k‐Means, G) Louvain Clustering, H) DBSCAN, and I) their corresponding AUCs.

Article Snippet: Antibodies against ATRN (Cat.: 202440‐T02), ORM2 (Cat.: 13299‐T16), SERPINA3 (Cat.: 10307‐RP02), and recombinant protein A (Cat.: 10600‐P07E) were acquired from Sino Biological.

Techniques:

Journal: iScience

Article Title: Pleiotropic brain function of whirlin identified by a novel mutation

doi: 10.1016/j.isci.2024.110170

Figure Lengend Snippet:

Article Snippet: Custom primers for TaqManTM reactions ( Col2741 Mm00508542_m1; Orm1 Mm00435456_g1; Orm2 Mm04213463_g1; Orm3 Mm03010552_g1, Akna Mm01258100_m1; Gapdh Mm99999915_g1, Ppia Mm02342429_g1, Actb Mm02619580_g1) used Fast Universal PCR Master Mix (2X) (ThermoFisher Scientific, UK).

Techniques: Reverse Transcription, Purification, SYBR Green Assay, TaqMan Assay, Sequencing, Generated, Software, Real-time Polymerase Chain Reaction, Microscopy

Reduced pancreatic ORM2 expression in AP. (A) Scatterplots showing log2 transformation of the normalized blood ORM1 in patients with MAP (n=57) and healthy controls (n=32). (B) Scatterplots showing log2 transformation of the normalized blood ORM2 in patients with MAP (n=57) and healthy controls (n=32). (C) The serum ORM in control and AP mice (n=6 per group). (D) Immunoblotting of ORM1 and ORM2 in serum from control and AP mice (n=6 per group). (E) Immunoblotting and quantitative analysis of ORM1 and ORM2 in pancreas from control and AP mice (n=6 per group). (F) Immunoblotting and quantitative analysis of ORM1 and ORM2 in liver from control and AP mice (n=6 per group). Data are presented as mean ± SEM. The groups were compared using unpaired two-tailed student’s t -test (*, P<0.05; ***, P<0.001; ****, P<0.0001). AP, acute pancreatitis; MAP, mild acute pancreatitis; ORM, orosomucoid; SEM, standard error of the mean.

Journal: Translational Gastroenterology and Hepatology

Article Title: ORM2 protects against acute pancreatitis by inhibiting premature activation of pancreatic enzymes

doi: 10.21037/tgh-25-106

Figure Lengend Snippet: Reduced pancreatic ORM2 expression in AP. (A) Scatterplots showing log2 transformation of the normalized blood ORM1 in patients with MAP (n=57) and healthy controls (n=32). (B) Scatterplots showing log2 transformation of the normalized blood ORM2 in patients with MAP (n=57) and healthy controls (n=32). (C) The serum ORM in control and AP mice (n=6 per group). (D) Immunoblotting of ORM1 and ORM2 in serum from control and AP mice (n=6 per group). (E) Immunoblotting and quantitative analysis of ORM1 and ORM2 in pancreas from control and AP mice (n=6 per group). (F) Immunoblotting and quantitative analysis of ORM1 and ORM2 in liver from control and AP mice (n=6 per group). Data are presented as mean ± SEM. The groups were compared using unpaired two-tailed student’s t -test (*, P<0.05; ***, P<0.001; ****, P<0.0001). AP, acute pancreatitis; MAP, mild acute pancreatitis; ORM, orosomucoid; SEM, standard error of the mean.

Article Snippet: The ORM2 (No. HY-P7490, MedChemExpress, New Jersey, USA) treatment was divided into low-dose and high-dose groups.

Techniques: Expressing, Transformation Assay, Control, Western Blot, Two Tailed Test

ORM2 deficiency contributes to AP progression. (A) The serum amylase level from ORM2 WT and ORM2 KO mice subjected to intraperitoneal injection of vehicle or caerulein (n=6 per group). (B) The serum IL-6 from ORM2 WT and ORM2 KO mice subjected to intraperitoneal injection of vehicle or caerulein (n=6 per group). (C) The serum TNF-α from ORM2 WT and ORM2 KO mice subjected to intraperitoneal injection of vehicle or caerulein (n=6 per group). (D) Representative HE staining and histological scores of the pancreatic tissues in ORM2 WT and ORM2 KO mice subjected to intraperitoneal injection of vehicle or caerulein (n=6 per group). Scale bar: 50 µm. Data are presented as mean ± SEM. The groups were compared using one-way ANOVA with Tukey’s post hoc test (****, P<0.0001). ANOVA, analysis of variance; AP, acute pancreatitis; IL-6, interleukin-6; HE, hematoxylin and eosin; SEM, standard error of the mean; TNF-α, tumor necrosis factor-alpha.

Journal: Translational Gastroenterology and Hepatology

Article Title: ORM2 protects against acute pancreatitis by inhibiting premature activation of pancreatic enzymes

doi: 10.21037/tgh-25-106

Figure Lengend Snippet: ORM2 deficiency contributes to AP progression. (A) The serum amylase level from ORM2 WT and ORM2 KO mice subjected to intraperitoneal injection of vehicle or caerulein (n=6 per group). (B) The serum IL-6 from ORM2 WT and ORM2 KO mice subjected to intraperitoneal injection of vehicle or caerulein (n=6 per group). (C) The serum TNF-α from ORM2 WT and ORM2 KO mice subjected to intraperitoneal injection of vehicle or caerulein (n=6 per group). (D) Representative HE staining and histological scores of the pancreatic tissues in ORM2 WT and ORM2 KO mice subjected to intraperitoneal injection of vehicle or caerulein (n=6 per group). Scale bar: 50 µm. Data are presented as mean ± SEM. The groups were compared using one-way ANOVA with Tukey’s post hoc test (****, P<0.0001). ANOVA, analysis of variance; AP, acute pancreatitis; IL-6, interleukin-6; HE, hematoxylin and eosin; SEM, standard error of the mean; TNF-α, tumor necrosis factor-alpha.

Article Snippet: The ORM2 (No. HY-P7490, MedChemExpress, New Jersey, USA) treatment was divided into low-dose and high-dose groups.

Techniques: Injection, Staining

Exogenous ORM2 attenuates acinar cell injury in vitro . (A) The mRNA level of Il-1β in control and CCK-induced primary acinar cells following treatment with vehicle, low-dose ORM2, or high-dose ORM2 (n=6 per group). Low-dose ORM2: 5 µg/mL, high-dose ORM2: 10 µg/mL. (B) The mRNA level of Il-6 in control and CCK-induced primary acinar cells following treatment with vehicle, low-dose ORM2, or high-dose ORM2 (n=6 per group). (C) The mRNA level of Tnf-α in control and CCK-induced primary acinar cells following treatment with vehicle, low-dose ORM2, or high-dose ORM2 (n=6 per group). (D) The amylase level in control and CCK-induced primary acinar cells following treatment with vehicle, low-dose ORM2, or high-dose ORM2 (n=6 per group). Data are presented as mean ± SEM. The groups were compared using one-way ANOVA with Tukey’s post hoc test (ns, not significant; **, P<0.01; ****, P<0.0001). ANOVA, analysis of variance; CCK, cholecystokinin; SEM, standard error of the mean.

Journal: Translational Gastroenterology and Hepatology

Article Title: ORM2 protects against acute pancreatitis by inhibiting premature activation of pancreatic enzymes

doi: 10.21037/tgh-25-106

Figure Lengend Snippet: Exogenous ORM2 attenuates acinar cell injury in vitro . (A) The mRNA level of Il-1β in control and CCK-induced primary acinar cells following treatment with vehicle, low-dose ORM2, or high-dose ORM2 (n=6 per group). Low-dose ORM2: 5 µg/mL, high-dose ORM2: 10 µg/mL. (B) The mRNA level of Il-6 in control and CCK-induced primary acinar cells following treatment with vehicle, low-dose ORM2, or high-dose ORM2 (n=6 per group). (C) The mRNA level of Tnf-α in control and CCK-induced primary acinar cells following treatment with vehicle, low-dose ORM2, or high-dose ORM2 (n=6 per group). (D) The amylase level in control and CCK-induced primary acinar cells following treatment with vehicle, low-dose ORM2, or high-dose ORM2 (n=6 per group). Data are presented as mean ± SEM. The groups were compared using one-way ANOVA with Tukey’s post hoc test (ns, not significant; **, P<0.01; ****, P<0.0001). ANOVA, analysis of variance; CCK, cholecystokinin; SEM, standard error of the mean.

Article Snippet: The ORM2 (No. HY-P7490, MedChemExpress, New Jersey, USA) treatment was divided into low-dose and high-dose groups.

Techniques: In Vitro, Control

Recombinant ORM2 administration alleviates AP in vivo. (A) The mRNA levels of Il-1β , Il-6 , Tnf-α , F4/80 , Mpo in control and AP mice following treatment with vehicle, low-dose ORM2, or high-dose ORM2 (n=6 per group). (B) The serum amylase and lipase in control and AP mice following treatment with vehicle, low-dose ORM2, or high-dose ORM2 (n=6 per group). (C) Representative HE staining and histological scores of the pancreatic tissues in control and AP mice following treatment with vehicle, low-dose ORM2, or high-dose ORM2 (n=6 per group). Scale bar: 50 µm. (D) Representative immunohistochemical staining of the pancreatic tissues in control and AP mice following treatment with vehicle, low-dose ORM2, or high-dose ORM2 (n=6 per group). Scale bar: 50 µm. The groups were compared using one-way ANOVA with Tukey’s post hoc test (ns, not significant; **, P<0.01; ***, P<0.001; ****, P<0.0001). ANOVA, analysis of variance; AP, acute pancreatitis; OH, high-dose ORM2; OL, low-dose ORM2; MPO, myeloperoxidase.

Journal: Translational Gastroenterology and Hepatology

Article Title: ORM2 protects against acute pancreatitis by inhibiting premature activation of pancreatic enzymes

doi: 10.21037/tgh-25-106

Figure Lengend Snippet: Recombinant ORM2 administration alleviates AP in vivo. (A) The mRNA levels of Il-1β , Il-6 , Tnf-α , F4/80 , Mpo in control and AP mice following treatment with vehicle, low-dose ORM2, or high-dose ORM2 (n=6 per group). (B) The serum amylase and lipase in control and AP mice following treatment with vehicle, low-dose ORM2, or high-dose ORM2 (n=6 per group). (C) Representative HE staining and histological scores of the pancreatic tissues in control and AP mice following treatment with vehicle, low-dose ORM2, or high-dose ORM2 (n=6 per group). Scale bar: 50 µm. (D) Representative immunohistochemical staining of the pancreatic tissues in control and AP mice following treatment with vehicle, low-dose ORM2, or high-dose ORM2 (n=6 per group). Scale bar: 50 µm. The groups were compared using one-way ANOVA with Tukey’s post hoc test (ns, not significant; **, P<0.01; ***, P<0.001; ****, P<0.0001). ANOVA, analysis of variance; AP, acute pancreatitis; OH, high-dose ORM2; OL, low-dose ORM2; MPO, myeloperoxidase.

Article Snippet: The ORM2 (No. HY-P7490, MedChemExpress, New Jersey, USA) treatment was divided into low-dose and high-dose groups.

Techniques: Recombinant, In Vivo, Control, Staining, Immunohistochemical staining

ORM2 inhibits pancreatic inflammation by preventing premature trypsinogen activation. (A) Volcano plot of differentially expressed proteins between AP and control groups. (B) Volcano plot of differentially expressed proteins between AP + ORM2 and AP groups (ORM2, 100 µg/kg). (C) The mRNA levels of Spink1 in control and AP mice following treatment with vehicle, low-dose ORM2, or high-dose ORM2 (n=6 per group). (D) The mRNA levels of Prss2 in control and AP mice following treatment with vehicle, low-dose ORM2, or high-dose ORM2 (n=6 per group). (E) The trypsin activity in pancreatic tissues from control and AP mice following treatment with vehicle, low-dose ORM2, or high-dose ORM2 (n=6 per group). Data are presented as mean ± SEM. The groups were compared using one-way ANOVA with Tukey’s post hoc test (ns, not significant; *, P<0.05; **, P<0.01; ****, P<0.0001). ANOVA, analysis of variance; AP, acute pancreatitis; OH, high-dose ORM2; OL, low-dose ORM2; SEM, standard error of the mean.

Journal: Translational Gastroenterology and Hepatology

Article Title: ORM2 protects against acute pancreatitis by inhibiting premature activation of pancreatic enzymes

doi: 10.21037/tgh-25-106

Figure Lengend Snippet: ORM2 inhibits pancreatic inflammation by preventing premature trypsinogen activation. (A) Volcano plot of differentially expressed proteins between AP and control groups. (B) Volcano plot of differentially expressed proteins between AP + ORM2 and AP groups (ORM2, 100 µg/kg). (C) The mRNA levels of Spink1 in control and AP mice following treatment with vehicle, low-dose ORM2, or high-dose ORM2 (n=6 per group). (D) The mRNA levels of Prss2 in control and AP mice following treatment with vehicle, low-dose ORM2, or high-dose ORM2 (n=6 per group). (E) The trypsin activity in pancreatic tissues from control and AP mice following treatment with vehicle, low-dose ORM2, or high-dose ORM2 (n=6 per group). Data are presented as mean ± SEM. The groups were compared using one-way ANOVA with Tukey’s post hoc test (ns, not significant; *, P<0.05; **, P<0.01; ****, P<0.0001). ANOVA, analysis of variance; AP, acute pancreatitis; OH, high-dose ORM2; OL, low-dose ORM2; SEM, standard error of the mean.

Article Snippet: The ORM2 (No. HY-P7490, MedChemExpress, New Jersey, USA) treatment was divided into low-dose and high-dose groups.

Techniques: Activation Assay, Control, Activity Assay