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Cusabio recombinant fth1 protein

ACOD1/itaconate axis upregulates <t>FTH1</t> to mitigate oxidative stress in macrophages. A. Re-clustering of the Mc4 macrophage subpopulation based on AcoD1 expression identifies ACOD1 + and ACOD1 - subsets. B. KEGG pathway enrichment analysis shows the necroptosis pathway is most significantly enriched in ACOD1 + macrophages compared to ACOD1 - subsets. Top 5 enriched pathways shown. C. Differential gene expression analysis within the necroptosis pathway identifies FTH1 as the most upregulated gene in ACOD1 + macrophages. D. Quantitative comparison of FTH1 expression levels in scRNA-seq data between normal trachea group and granulation group. E, F. Representative images of FTH1 immunohistochemical staining and quantitative of immunoreactive area in normal trachea group and granulation group. Scale bars indicate 200 μm and 50 μm (n = 3 sample per group). G, H. Western blot analysis showing the levels of ACOD1 in the trachea of control group, BAS group and BAS+4-OI group (n = 3 mice per group) at 24 h. I, J. Representative tracheal immunofluorescence images and mean fluorescence intensity of FTH1(green) in control group, BAS group and BAS+4-OI group (n = 5 mice per group) at 24 h. Scale bars indicate 200 μm and 50 μm. K. Representative immunofluorescence images of CD68(red), FTH1(green) and ACOD1(yellow)in normal trachea group and granulation group. Scale bars indicate 200 μm and 50 μm. L. Representative tracheal immunofluorescence images of F4/80(red), FTH1(green) and ACOD1(yellow)in control group and BAS group. Scale bars indicate 200 μm and 50 μm. M, N. Western blot analysis in macrophages reveals that 4-OI rescues LPS-induced FTH1 downregulation (n = 3 independent experiments). O, P. Representative immunofluorescence images and mean fluorescence intensity of ROS (red) in 4-OI reduces LPS-induced 4-HNE in controls, but not in FTH1-knockdown macrophages. (n = 3 independent experiments). Scale bars indicate 50 μm. Q, R. Western blot and quantitative analysis of FTH1 in macrophages after transfection with siNRF2 and treated or not with 4-OI, LPS (n = 3 independent experiments). Data are presented as the mean ± SEM. Two-sided student's T-test were used in D,F. One-way ANOVA analysis followed by Tukey post hoc multi-comparison test was used in H, J. Two-way ANOVA analysis followed by Tukey post hoc multi-comparison test was used in N, P, R.

Recombinant Fth1 Protein, supplied by Cusabio, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/recombinant+fth1+protein/pmc13010451-363-8-11?v=Cusabio
Average 94 stars, based on 1 article reviews

recombinant fth1 protein - by Bioz Stars, 2026-08

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1) Product Images from "ACOD-itaconate in macrophage attenuates oxidative stress and inflammation in benign airway stenosis by upregulating and transferring FTH1"

Article Title: ACOD-itaconate in macrophage attenuates oxidative stress and inflammation in benign airway stenosis by upregulating and transferring FTH1

Journal: Redox Biology

doi: 10.1016/j.redox.2026.104133

ACOD1/itaconate axis upregulates FTH1 to mitigate oxidative stress in macrophages. A. Re-clustering of the Mc4 macrophage subpopulation based on AcoD1 expression identifies ACOD1 + and ACOD1 - subsets. B. KEGG pathway enrichment analysis shows the necroptosis pathway is most significantly enriched in ACOD1 + macrophages compared to ACOD1 - subsets. Top 5 enriched pathways shown. C. Differential gene expression analysis within the necroptosis pathway identifies FTH1 as the most upregulated gene in ACOD1 + macrophages. D. Quantitative comparison of FTH1 expression levels in scRNA-seq data between normal trachea group and granulation group. E, F. Representative images of FTH1 immunohistochemical staining and quantitative of immunoreactive area in normal trachea group and granulation group. Scale bars indicate 200 μm and 50 μm (n = 3 sample per group). G, H. Western blot analysis showing the levels of ACOD1 in the trachea of control group, BAS group and BAS+4-OI group (n = 3 mice per group) at 24 h. I, J. Representative tracheal immunofluorescence images and mean fluorescence intensity of FTH1(green) in control group, BAS group and BAS+4-OI group (n = 5 mice per group) at 24 h. Scale bars indicate 200 μm and 50 μm. K. Representative immunofluorescence images of CD68(red), FTH1(green) and ACOD1(yellow)in normal trachea group and granulation group. Scale bars indicate 200 μm and 50 μm. L. Representative tracheal immunofluorescence images of F4/80(red), FTH1(green) and ACOD1(yellow)in control group and BAS group. Scale bars indicate 200 μm and 50 μm. M, N. Western blot analysis in macrophages reveals that 4-OI rescues LPS-induced FTH1 downregulation (n = 3 independent experiments). O, P. Representative immunofluorescence images and mean fluorescence intensity of ROS (red) in 4-OI reduces LPS-induced 4-HNE in controls, but not in FTH1-knockdown macrophages. (n = 3 independent experiments). Scale bars indicate 50 μm. Q, R. Western blot and quantitative analysis of FTH1 in macrophages after transfection with siNRF2 and treated or not with 4-OI, LPS (n = 3 independent experiments). Data are presented as the mean ± SEM. Two-sided student's T-test were used in D,F. One-way ANOVA analysis followed by Tukey post hoc multi-comparison test was used in H, J. Two-way ANOVA analysis followed by Tukey post hoc multi-comparison test was used in N, P, R.

Figure Legend Snippet: ACOD1/itaconate axis upregulates FTH1 to mitigate oxidative stress in macrophages. A. Re-clustering of the Mc4 macrophage subpopulation based on AcoD1 expression identifies ACOD1 + and ACOD1 - subsets. B. KEGG pathway enrichment analysis shows the necroptosis pathway is most significantly enriched in ACOD1 + macrophages compared to ACOD1 - subsets. Top 5 enriched pathways shown. C. Differential gene expression analysis within the necroptosis pathway identifies FTH1 as the most upregulated gene in ACOD1 + macrophages. D. Quantitative comparison of FTH1 expression levels in scRNA-seq data between normal trachea group and granulation group. E, F. Representative images of FTH1 immunohistochemical staining and quantitative of immunoreactive area in normal trachea group and granulation group. Scale bars indicate 200 μm and 50 μm (n = 3 sample per group). G, H. Western blot analysis showing the levels of ACOD1 in the trachea of control group, BAS group and BAS+4-OI group (n = 3 mice per group) at 24 h. I, J. Representative tracheal immunofluorescence images and mean fluorescence intensity of FTH1(green) in control group, BAS group and BAS+4-OI group (n = 5 mice per group) at 24 h. Scale bars indicate 200 μm and 50 μm. K. Representative immunofluorescence images of CD68(red), FTH1(green) and ACOD1(yellow)in normal trachea group and granulation group. Scale bars indicate 200 μm and 50 μm. L. Representative tracheal immunofluorescence images of F4/80(red), FTH1(green) and ACOD1(yellow)in control group and BAS group. Scale bars indicate 200 μm and 50 μm. M, N. Western blot analysis in macrophages reveals that 4-OI rescues LPS-induced FTH1 downregulation (n = 3 independent experiments). O, P. Representative immunofluorescence images and mean fluorescence intensity of ROS (red) in 4-OI reduces LPS-induced 4-HNE in controls, but not in FTH1-knockdown macrophages. (n = 3 independent experiments). Scale bars indicate 50 μm. Q, R. Western blot and quantitative analysis of FTH1 in macrophages after transfection with siNRF2 and treated or not with 4-OI, LPS (n = 3 independent experiments). Data are presented as the mean ± SEM. Two-sided student's T-test were used in D,F. One-way ANOVA analysis followed by Tukey post hoc multi-comparison test was used in H, J. Two-way ANOVA analysis followed by Tukey post hoc multi-comparison test was used in N, P, R.

Techniques Used: Expressing, Gene Expression, Comparison, Immunohistochemical staining, Staining, Western Blot, Control, Immunofluorescence, Fluorescence, Knockdown, Transfection

4-OI promotes exosomal FTH1 secretion from macrophages and induces fibroblast ferroptosis. A. ELISA detects elevated FTH1 secretion in supernatants of macrophages treated with LPS + 4-OI, but not 4-OI alone (n = 3 independent experiments). B. Representative TEM images of exosomes isolated from LPS+4-OI treated macrophages. Scale bars indicate 500 nm and 200 nm. C. Representative NTA of exosomes isolated from LPS+4-OI treated macrophages. D. Representative immunoblot shows exosome markers (TSG101, CD63, and CD81) and endoplasmic reticulum marker (Calnexin). E. Schematic diagram of exosome uptake experiment. F. Representative immunofluorescence images of DiD (red) and F-actin (green) in two fibroblasts group. Scale bars indicate 20 μm. G. Representative immunoblot shows FTH1 and CD63 in two EXO group. H,I. Representative immunofluorescence images and mean fluorescence intensity of FTH1 (red) in three fibroblasts group (n = 3 independent experiments). Scale bars indicate 50 μm. J. Experimental scheme: Macrophage-fibroblast co-culture system. K,L. Representative immunofluorescence images and mean fluorescence show co-culture with macrophages treated with LPS+4-OI significantly enhanced FTH1 internalization in fibroblasts. This effect was abolished when macrophages were subjected to FTH1 knockdown (LPS+4-OI + siFTH1), and was restored upon addition of recombinant FTH1 (LPS+4-OI + siFTH1+rFTH1) (n = 3 independent experiments). Scale bars indicate 50 μm. M,N. Representative immunofluorescence images and mean fluorescence of PGSK in fibroblasts after co-culture with the indicated macrophage groups: control, LPS+4-OI, LPS+4-OI + siFTH1, and LPS+4-OI + siFTH1+rFTH1 (n = 3 independent experiments). Scale bars indicate 100 μm. O,P. Representative immunofluorescence images and Mean fluorescence intensity of BODIPY C11(red) and oxidized form(green) in two group(n = 3 independent experiments) Scale bars indicate 50 μm. Q. Representative TEM images of differently treated fibroblasts group. Scale bars indicate 2 μm and 500 nm. R,S. Representative immunofluorescence images and mean fluorescence intensity of 4HNE (red) in three fibroblasts group (n = 3 independent experiments). Scale bars indicate 50 μm. Data are presented as the mean ± SEM. Two-sided student's T-test were used in P. One-way ANOVA analysis followed by Tukey post hoc multi-comparison test was used in A,I,L,N,S .

Figure Legend Snippet: 4-OI promotes exosomal FTH1 secretion from macrophages and induces fibroblast ferroptosis. A. ELISA detects elevated FTH1 secretion in supernatants of macrophages treated with LPS + 4-OI, but not 4-OI alone (n = 3 independent experiments). B. Representative TEM images of exosomes isolated from LPS+4-OI treated macrophages. Scale bars indicate 500 nm and 200 nm. C. Representative NTA of exosomes isolated from LPS+4-OI treated macrophages. D. Representative immunoblot shows exosome markers (TSG101, CD63, and CD81) and endoplasmic reticulum marker (Calnexin). E. Schematic diagram of exosome uptake experiment. F. Representative immunofluorescence images of DiD (red) and F-actin (green) in two fibroblasts group. Scale bars indicate 20 μm. G. Representative immunoblot shows FTH1 and CD63 in two EXO group. H,I. Representative immunofluorescence images and mean fluorescence intensity of FTH1 (red) in three fibroblasts group (n = 3 independent experiments). Scale bars indicate 50 μm. J. Experimental scheme: Macrophage-fibroblast co-culture system. K,L. Representative immunofluorescence images and mean fluorescence show co-culture with macrophages treated with LPS+4-OI significantly enhanced FTH1 internalization in fibroblasts. This effect was abolished when macrophages were subjected to FTH1 knockdown (LPS+4-OI + siFTH1), and was restored upon addition of recombinant FTH1 (LPS+4-OI + siFTH1+rFTH1) (n = 3 independent experiments). Scale bars indicate 50 μm. M,N. Representative immunofluorescence images and mean fluorescence of PGSK in fibroblasts after co-culture with the indicated macrophage groups: control, LPS+4-OI, LPS+4-OI + siFTH1, and LPS+4-OI + siFTH1+rFTH1 (n = 3 independent experiments). Scale bars indicate 100 μm. O,P. Representative immunofluorescence images and Mean fluorescence intensity of BODIPY C11(red) and oxidized form(green) in two group(n = 3 independent experiments) Scale bars indicate 50 μm. Q. Representative TEM images of differently treated fibroblasts group. Scale bars indicate 2 μm and 500 nm. R,S. Representative immunofluorescence images and mean fluorescence intensity of 4HNE (red) in three fibroblasts group (n = 3 independent experiments). Scale bars indicate 50 μm. Data are presented as the mean ± SEM. Two-sided student's T-test were used in P. One-way ANOVA analysis followed by Tukey post hoc multi-comparison test was used in A,I,L,N,S .

Techniques Used: Enzyme-linked Immunosorbent Assay, Isolation, Western Blot, Marker, Immunofluorescence, Fluorescence, Co-Culture Assay, Knockdown, Recombinant, Control, Comparison

Macrophage-derived FTH1 binds fibroblast SCARA5 to inhibit fibrosis. A. Re-clustering of fibroblasts from single-cell RNA-seq data identifies distinct subpopulations in human BAS granulation tissue. B. Pseudotime trajectory analysis reveals fibroblast differentiation converging on pro-fibrotic Cluster 2. C. CellChat interaction analysis predicts FTH1 (from ACOD1 + macrophages) binding to SCARA5 (on Cluster 2 fibroblasts) as the top ligand-receptor pair. D. Representative immunofluorescence images of FTH1(green), SCARA5(yellow) and Vimentin (red) in normal trachea group and granulation group. Scale bars indicate 50 μm and 20 μm. E. Co-immunoprecipitation (Co-IP) confirms FTH1 binding to SCARA5 in fibroblasts co-cultured with LPS+4-OI-treated macrophages. F,G. Representative tracheal immunofluorescence images of FTH1 (green), GPX4(yellow), SCARA5(red) and VIMENTIN(pink) in mouse trachea and quantitative of mean fluorescence of FTH1 and GPX4 in the control, BAS and BAS+4-OI group(n = 3 mice per group). Scale bars indicate 200 μm and 50 μm. H. Schematic diagram of the experimental design for 4-OI and Anti -SCARA5 treatment. I,J. Representative immunofluorescence images and mean fluorescence intensity of αSMA (red) and COL1(green) in four group: Control, BAS,BAS+4-OI,BAS+4-OI + Anti -SCARA5 (n = 3 mice per group). Scale bars indicate 200 μm and 50 μm. Data are presented as the mean ± SEM. One-way ANOVA analysis followed by Tukey post hoc multi-comparison test was used in G, J.

Figure Legend Snippet: Macrophage-derived FTH1 binds fibroblast SCARA5 to inhibit fibrosis. A. Re-clustering of fibroblasts from single-cell RNA-seq data identifies distinct subpopulations in human BAS granulation tissue. B. Pseudotime trajectory analysis reveals fibroblast differentiation converging on pro-fibrotic Cluster 2. C. CellChat interaction analysis predicts FTH1 (from ACOD1 + macrophages) binding to SCARA5 (on Cluster 2 fibroblasts) as the top ligand-receptor pair. D. Representative immunofluorescence images of FTH1(green), SCARA5(yellow) and Vimentin (red) in normal trachea group and granulation group. Scale bars indicate 50 μm and 20 μm. E. Co-immunoprecipitation (Co-IP) confirms FTH1 binding to SCARA5 in fibroblasts co-cultured with LPS+4-OI-treated macrophages. F,G. Representative tracheal immunofluorescence images of FTH1 (green), GPX4(yellow), SCARA5(red) and VIMENTIN(pink) in mouse trachea and quantitative of mean fluorescence of FTH1 and GPX4 in the control, BAS and BAS+4-OI group(n = 3 mice per group). Scale bars indicate 200 μm and 50 μm. H. Schematic diagram of the experimental design for 4-OI and Anti -SCARA5 treatment. I,J. Representative immunofluorescence images and mean fluorescence intensity of αSMA (red) and COL1(green) in four group: Control, BAS,BAS+4-OI,BAS+4-OI + Anti -SCARA5 (n = 3 mice per group). Scale bars indicate 200 μm and 50 μm. Data are presented as the mean ± SEM. One-way ANOVA analysis followed by Tukey post hoc multi-comparison test was used in G, J.

Techniques Used: Derivative Assay, Single Cell, RNA Sequencing, Binding Assay, Immunofluorescence, Immunoprecipitation, Co-Immunoprecipitation Assay, Cell Culture, Fluorescence, Control, Comparison

Schematic diagram of mechanism of the ACOD1/itaconate axis in regulating airway inflammation and fibrosis. During the inflammatory stage, macrophages upregulate ACOD1 expression, catalyzing itaconate production. Itaconate and its derivative 4-OI activate the NRF2 signaling pathway by promoting NRF2 nuclear translocation. Nuclear NRF2 induces FTH1 transcription, leading to intracellular FTH1 protein accumulation to suppressing inflammation and attenuating oxidative stress. In fibrotic repair, FTH1 packaged into exosomes and secreted. These exosomes are taken up by fibroblasts via bind to SCARA5, leading to FTH1 delivery and subsequent induction of ferroptosis.

Figure Legend Snippet: Schematic diagram of mechanism of the ACOD1/itaconate axis in regulating airway inflammation and fibrosis. During the inflammatory stage, macrophages upregulate ACOD1 expression, catalyzing itaconate production. Itaconate and its derivative 4-OI activate the NRF2 signaling pathway by promoting NRF2 nuclear translocation. Nuclear NRF2 induces FTH1 transcription, leading to intracellular FTH1 protein accumulation to suppressing inflammation and attenuating oxidative stress. In fibrotic repair, FTH1 packaged into exosomes and secreted. These exosomes are taken up by fibroblasts via bind to SCARA5, leading to FTH1 delivery and subsequent induction of ferroptosis.

Techniques Used: Expressing, Translocation Assay

Image Search Results

Journal: Redox Biology

Article Title: ACOD-itaconate in macrophage attenuates oxidative stress and inflammation in benign airway stenosis by upregulating and transferring FTH1

doi: 10.1016/j.redox.2026.104133

Figure Lengend Snippet: ACOD1/itaconate axis upregulates FTH1 to mitigate oxidative stress in macrophages. A. Re-clustering of the Mc4 macrophage subpopulation based on AcoD1 expression identifies ACOD1 + and ACOD1 - subsets. B. KEGG pathway enrichment analysis shows the necroptosis pathway is most significantly enriched in ACOD1 + macrophages compared to ACOD1 - subsets. Top 5 enriched pathways shown. C. Differential gene expression analysis within the necroptosis pathway identifies FTH1 as the most upregulated gene in ACOD1 + macrophages. D. Quantitative comparison of FTH1 expression levels in scRNA-seq data between normal trachea group and granulation group. E, F. Representative images of FTH1 immunohistochemical staining and quantitative of immunoreactive area in normal trachea group and granulation group. Scale bars indicate 200 μm and 50 μm (n = 3 sample per group). G, H. Western blot analysis showing the levels of ACOD1 in the trachea of control group, BAS group and BAS+4-OI group (n = 3 mice per group) at 24 h. I, J. Representative tracheal immunofluorescence images and mean fluorescence intensity of FTH1(green) in control group, BAS group and BAS+4-OI group (n = 5 mice per group) at 24 h. Scale bars indicate 200 μm and 50 μm. K. Representative immunofluorescence images of CD68(red), FTH1(green) and ACOD1(yellow)in normal trachea group and granulation group. Scale bars indicate 200 μm and 50 μm. L. Representative tracheal immunofluorescence images of F4/80(red), FTH1(green) and ACOD1(yellow)in control group and BAS group. Scale bars indicate 200 μm and 50 μm. M, N. Western blot analysis in macrophages reveals that 4-OI rescues LPS-induced FTH1 downregulation (n = 3 independent experiments). O, P. Representative immunofluorescence images and mean fluorescence intensity of ROS (red) in 4-OI reduces LPS-induced 4-HNE in controls, but not in FTH1-knockdown macrophages. (n = 3 independent experiments). Scale bars indicate 50 μm. Q, R. Western blot and quantitative analysis of FTH1 in macrophages after transfection with siNRF2 and treated or not with 4-OI, LPS (n = 3 independent experiments). Data are presented as the mean ± SEM. Two-sided student's T-test were used in D,F. One-way ANOVA analysis followed by Tukey post hoc multi-comparison test was used in H, J. Two-way ANOVA analysis followed by Tukey post hoc multi-comparison test was used in N, P, R.

Article Snippet: For add exogenous FTH1, fibroblasts were treated with recombinant FTH1 protein(#CSB-EP009030MO, cusabio).

Techniques: Expressing, Gene Expression, Comparison, Immunohistochemical staining, Staining, Western Blot, Control, Immunofluorescence, Fluorescence, Knockdown, Transfection

Journal: Redox Biology

Article Title: ACOD-itaconate in macrophage attenuates oxidative stress and inflammation in benign airway stenosis by upregulating and transferring FTH1

doi: 10.1016/j.redox.2026.104133

Figure Lengend Snippet: 4-OI promotes exosomal FTH1 secretion from macrophages and induces fibroblast ferroptosis. A. ELISA detects elevated FTH1 secretion in supernatants of macrophages treated with LPS + 4-OI, but not 4-OI alone (n = 3 independent experiments). B. Representative TEM images of exosomes isolated from LPS+4-OI treated macrophages. Scale bars indicate 500 nm and 200 nm. C. Representative NTA of exosomes isolated from LPS+4-OI treated macrophages. D. Representative immunoblot shows exosome markers (TSG101, CD63, and CD81) and endoplasmic reticulum marker (Calnexin). E. Schematic diagram of exosome uptake experiment. F. Representative immunofluorescence images of DiD (red) and F-actin (green) in two fibroblasts group. Scale bars indicate 20 μm. G. Representative immunoblot shows FTH1 and CD63 in two EXO group. H,I. Representative immunofluorescence images and mean fluorescence intensity of FTH1 (red) in three fibroblasts group (n = 3 independent experiments). Scale bars indicate 50 μm. J. Experimental scheme: Macrophage-fibroblast co-culture system. K,L. Representative immunofluorescence images and mean fluorescence show co-culture with macrophages treated with LPS+4-OI significantly enhanced FTH1 internalization in fibroblasts. This effect was abolished when macrophages were subjected to FTH1 knockdown (LPS+4-OI + siFTH1), and was restored upon addition of recombinant FTH1 (LPS+4-OI + siFTH1+rFTH1) (n = 3 independent experiments). Scale bars indicate 50 μm. M,N. Representative immunofluorescence images and mean fluorescence of PGSK in fibroblasts after co-culture with the indicated macrophage groups: control, LPS+4-OI, LPS+4-OI + siFTH1, and LPS+4-OI + siFTH1+rFTH1 (n = 3 independent experiments). Scale bars indicate 100 μm. O,P. Representative immunofluorescence images and Mean fluorescence intensity of BODIPY C11(red) and oxidized form(green) in two group(n = 3 independent experiments) Scale bars indicate 50 μm. Q. Representative TEM images of differently treated fibroblasts group. Scale bars indicate 2 μm and 500 nm. R,S. Representative immunofluorescence images and mean fluorescence intensity of 4HNE (red) in three fibroblasts group (n = 3 independent experiments). Scale bars indicate 50 μm. Data are presented as the mean ± SEM. Two-sided student's T-test were used in P. One-way ANOVA analysis followed by Tukey post hoc multi-comparison test was used in A,I,L,N,S .

Article Snippet: For add exogenous FTH1, fibroblasts were treated with recombinant FTH1 protein(#CSB-EP009030MO, cusabio).

Techniques: Enzyme-linked Immunosorbent Assay, Isolation, Western Blot, Marker, Immunofluorescence, Fluorescence, Co-Culture Assay, Knockdown, Recombinant, Control, Comparison

Journal: Redox Biology

Article Title: ACOD-itaconate in macrophage attenuates oxidative stress and inflammation in benign airway stenosis by upregulating and transferring FTH1

doi: 10.1016/j.redox.2026.104133

Figure Lengend Snippet: Macrophage-derived FTH1 binds fibroblast SCARA5 to inhibit fibrosis. A. Re-clustering of fibroblasts from single-cell RNA-seq data identifies distinct subpopulations in human BAS granulation tissue. B. Pseudotime trajectory analysis reveals fibroblast differentiation converging on pro-fibrotic Cluster 2. C. CellChat interaction analysis predicts FTH1 (from ACOD1 + macrophages) binding to SCARA5 (on Cluster 2 fibroblasts) as the top ligand-receptor pair. D. Representative immunofluorescence images of FTH1(green), SCARA5(yellow) and Vimentin (red) in normal trachea group and granulation group. Scale bars indicate 50 μm and 20 μm. E. Co-immunoprecipitation (Co-IP) confirms FTH1 binding to SCARA5 in fibroblasts co-cultured with LPS+4-OI-treated macrophages. F,G. Representative tracheal immunofluorescence images of FTH1 (green), GPX4(yellow), SCARA5(red) and VIMENTIN(pink) in mouse trachea and quantitative of mean fluorescence of FTH1 and GPX4 in the control, BAS and BAS+4-OI group(n = 3 mice per group). Scale bars indicate 200 μm and 50 μm. H. Schematic diagram of the experimental design for 4-OI and Anti -SCARA5 treatment. I,J. Representative immunofluorescence images and mean fluorescence intensity of αSMA (red) and COL1(green) in four group: Control, BAS,BAS+4-OI,BAS+4-OI + Anti -SCARA5 (n = 3 mice per group). Scale bars indicate 200 μm and 50 μm. Data are presented as the mean ± SEM. One-way ANOVA analysis followed by Tukey post hoc multi-comparison test was used in G, J.

Article Snippet: For add exogenous FTH1, fibroblasts were treated with recombinant FTH1 protein(#CSB-EP009030MO, cusabio).

Techniques: Derivative Assay, Single Cell, RNA Sequencing, Binding Assay, Immunofluorescence, Immunoprecipitation, Co-Immunoprecipitation Assay, Cell Culture, Fluorescence, Control, Comparison

Journal: Redox Biology

Article Title: ACOD-itaconate in macrophage attenuates oxidative stress and inflammation in benign airway stenosis by upregulating and transferring FTH1

doi: 10.1016/j.redox.2026.104133

Figure Lengend Snippet: Schematic diagram of mechanism of the ACOD1/itaconate axis in regulating airway inflammation and fibrosis. During the inflammatory stage, macrophages upregulate ACOD1 expression, catalyzing itaconate production. Itaconate and its derivative 4-OI activate the NRF2 signaling pathway by promoting NRF2 nuclear translocation. Nuclear NRF2 induces FTH1 transcription, leading to intracellular FTH1 protein accumulation to suppressing inflammation and attenuating oxidative stress. In fibrotic repair, FTH1 packaged into exosomes and secreted. These exosomes are taken up by fibroblasts via bind to SCARA5, leading to FTH1 delivery and subsequent induction of ferroptosis.

Article Snippet: For add exogenous FTH1, fibroblasts were treated with recombinant FTH1 protein(#CSB-EP009030MO, cusabio).

Techniques: Expressing, Translocation Assay

FTH1 serves as a crucial target for OP-D in promoting ferroptosis in lung fibroblasts. A Heatmap of ferroptosis-related protein expression before and after OP-D treatment. B The mRNA expression of FTH1, GPX4, and SLC7A11 in different cell groups, n = 3. C , D Western blotting and quantification of protein expression for FTH1, GPX4, and SLC7A11 in diverse cell groups. E Binding Efficiency of the OP-D to FTH1, GPX4 and SLC7A11 Molecules. F The interaction pattern between the FTH1 protein and OP-D. G Immunofluorescence colocalization of FTH1 in human lung fibroblasts treated with varying concentrations of OP-D, with quantification of immunolabeled areas across treatment groups, Scale bar = 20 μm. Data expressed as mean ± SD; ###, p < 0.001 versus Control group; ***, p < 0.001, **, p < 0.01, *, p < 0.05, ns, not significant versus TGF-β group

Journal: Chinese Medicine

Article Title: Maimendong decoction and its active ingredient, ophiopogonin D, alleviate bleomycin-induced pulmonary fibrosis by regulating the behavior of lung fibroblasts

doi: 10.1186/s13020-025-01206-x

Figure Lengend Snippet: FTH1 serves as a crucial target for OP-D in promoting ferroptosis in lung fibroblasts. A Heatmap of ferroptosis-related protein expression before and after OP-D treatment. B The mRNA expression of FTH1, GPX4, and SLC7A11 in different cell groups, n = 3. C , D Western blotting and quantification of protein expression for FTH1, GPX4, and SLC7A11 in diverse cell groups. E Binding Efficiency of the OP-D to FTH1, GPX4 and SLC7A11 Molecules. F The interaction pattern between the FTH1 protein and OP-D. G Immunofluorescence colocalization of FTH1 in human lung fibroblasts treated with varying concentrations of OP-D, with quantification of immunolabeled areas across treatment groups, Scale bar = 20 μm. Data expressed as mean ± SD; ###, p < 0.001 versus Control group; ***, p < 0.001, **, p < 0.01, *, p < 0.05, ns, not significant versus TGF-β group

Article Snippet: FTH1 , Boster , BM4487 , 1:1000.

Techniques: Expressing, Western Blot, Binding Assay, Immunofluorescence, Immunolabeling, Control

Overexpression of FTH1 can eliminate the effect of OP-D in promoting ferroptosis in lung fibroblasts. A , B Western blotting and quantitative evaluation of how varying concentrations of OP-D influence FTH1 protein expression in HFL1 cells without TGF-β stimulation. C The mRNA expression of FTH1 in different cell groups. D The qPCR detection of the mRNA expression after overexpression of FTH1. E , F Western blotting and the quantitative evaluation of the protein expressions of FTH1, α-SMA, Collagen I, Transferrin, and Vimentin after the overexpression of FTH1. G Cell proliferation rates were assessed using the CCK8 assay. H Immunofluorescence analysis showed colocalization of FTH1 and GPX4, with quantification of their immunolabeled areas across different treatment groups, Scale bar = 20 μm. Data expressed as mean ± SD; ###, p < 0.001, ##, p < 0.01, ns, not significant versus Control group; ***, p < 0.001, **, p < 0.01, *, p < 0.05, ns, not significant versus TGF-β group. + + +, p < 0.001, + +, p < 0.01, +, p < 0.05 versus TGF-β + OP-D (10 μM) + oe-NC group

Journal: Chinese Medicine

Article Title: Maimendong decoction and its active ingredient, ophiopogonin D, alleviate bleomycin-induced pulmonary fibrosis by regulating the behavior of lung fibroblasts

doi: 10.1186/s13020-025-01206-x

Figure Lengend Snippet: Overexpression of FTH1 can eliminate the effect of OP-D in promoting ferroptosis in lung fibroblasts. A , B Western blotting and quantitative evaluation of how varying concentrations of OP-D influence FTH1 protein expression in HFL1 cells without TGF-β stimulation. C The mRNA expression of FTH1 in different cell groups. D The qPCR detection of the mRNA expression after overexpression of FTH1. E , F Western blotting and the quantitative evaluation of the protein expressions of FTH1, α-SMA, Collagen I, Transferrin, and Vimentin after the overexpression of FTH1. G Cell proliferation rates were assessed using the CCK8 assay. H Immunofluorescence analysis showed colocalization of FTH1 and GPX4, with quantification of their immunolabeled areas across different treatment groups, Scale bar = 20 μm. Data expressed as mean ± SD; ###, p < 0.001, ##, p < 0.01, ns, not significant versus Control group; ***, p < 0.001, **, p < 0.01, *, p < 0.05, ns, not significant versus TGF-β group. + + +, p < 0.001, + +, p < 0.01, +, p < 0.05 versus TGF-β + OP-D (10 μM) + oe-NC group

Article Snippet: FTH1 , Boster , BM4487 , 1:1000.

Techniques: Over Expression, Western Blot, Expressing, CCK-8 Assay, Immunofluorescence, Immunolabeling, Control

MMDD and its principal active constituent, OP-D, alleviate pulmonary fibrosis through targeting lung fibroblasts. Both MMDD and OP-D exhibit anti-fibrotic properties by inhibiting the TGF-β signaling pathway, reducing fibroblast proliferation, and inducing ferroptosis, while suppression of FTH1 expression is recognized as a critical target

Journal: Chinese Medicine

Article Title: Maimendong decoction and its active ingredient, ophiopogonin D, alleviate bleomycin-induced pulmonary fibrosis by regulating the behavior of lung fibroblasts

doi: 10.1186/s13020-025-01206-x

Figure Lengend Snippet: MMDD and its principal active constituent, OP-D, alleviate pulmonary fibrosis through targeting lung fibroblasts. Both MMDD and OP-D exhibit anti-fibrotic properties by inhibiting the TGF-β signaling pathway, reducing fibroblast proliferation, and inducing ferroptosis, while suppression of FTH1 expression is recognized as a critical target

Article Snippet: FTH1 , Boster , BM4487 , 1:1000.

Techniques: Expressing

Figure 3. (A) Ultra-structure of hepatocytes near cysts at different stages of infection with PSCs (0, 1, 3, and 6 months); mitochondria are indicated by white arrows,PSC are indicated by black arrows(n = 3 rats/group, scale bars represent 2 µm and 1 µm). (B) Fe2+, (C) GSH, (D(a,b)) ROS, (E) MDA, (F) SOD, and (G) LDH of hepatocytes near cysts at different stages of infection with PSCs. (H(a,b)) Western blotting of protein expression levels of TFRC, GPX4, FTH1, NOX1, SLC3A2, and SLC7A11 in ferroptosis signaling pathway in rat liver tissue at different stages of infection with PSCs (n = 3 rats/group)); * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 (Student t test).

Journal: Cells

Article Title: Echinococcus granulosus -Induced Liver Damage Through Ferroptosis in Rat Model.

doi: 10.3390/cells14050328

Figure Lengend Snippet: Figure 3. (A) Ultra-structure of hepatocytes near cysts at different stages of infection with PSCs (0, 1, 3, and 6 months); mitochondria are indicated by white arrows,PSC are indicated by black arrows(n = 3 rats/group, scale bars represent 2 µm and 1 µm). (B) Fe2+, (C) GSH, (D(a,b)) ROS, (E) MDA, (F) SOD, and (G) LDH of hepatocytes near cysts at different stages of infection with PSCs. (H(a,b)) Western blotting of protein expression levels of TFRC, GPX4, FTH1, NOX1, SLC3A2, and SLC7A11 in ferroptosis signaling pathway in rat liver tissue at different stages of infection with PSCs (n = 3 rats/group)); * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 (Student t test).

Article Snippet: The antibodies used in this study were as follows: TFRC (Boster, 1: 500, Rabbit, BA0462-2, Wuhan, China); Caspase-3 (Boster, 1:500, Rabbit, BA3257, Wuhan, China); Cells 2025, 14, 328 6 of 16 GSDMD (Proteintech Group, 1:800, Rabbit, 20770-1-AP, Wuhan, China); LC3I/II (Abcam, 1:1000, Rabbit, ab192890, Shanghai, China); Anti-GPX4 Antibody (Boster, 1:400, Rabbit, BM5231,Wuhan, China); Anti-FTH1 Antibody (Boster, China, 1:400, Rabbit, BM4487,Wuhan, China); Anti-NOX1 Antibody (Boster, China, 1:400, Rabbit, BA3720,Wuhan, China); AntiCD98 Antibody (SLC3A2, Boster, China, 1:400, Rabbit, A01794-1,Wuhan,China); AntixCT Antibody (SLC7A11,Abcam,1:400, Rabbit, A01794-1, Shanghai, China); β-actin (Sino Biological, 1:1000, Mouse, 100166-MM10, Beijing, China).

Techniques: Infection, Western Blot, Expressing

Figure 4. (A) Ferrostatin-1 inhibitor intervenes in vivo in PSC-mediated hepatocyte ferroptosis model establishment. (B) Characteristics of rat liver cyst morphology in rat blank control group, 1-month infection model group, and Ferrostatin-1 (5 mg/kg) intervention group. Cysts are indicated by white arrows (n = 6 rats/group). (C) Histological changes in Ferrostatin-1 on liver cysts in a rat model infected with PSCs for 1 month; germinal layer, keratinization layer, and inflammatory cell zone are indicated by black, white, and blue arrows (n = 6 rats/group; scale bars represent 100 µm and 50 µm). (D) TEM observation of Ferrostatin-1 on cyst peripheral hepatocyte ultra-structure changes in a rat model infected with PSCs for 1 month; mitochondria are indicated by white arrows (n = 3 rats/group; scale bars represent 2 µm and 1 µm). Effect of Ferrostatin-1 on (E) Fe2+, (F) GSH, (G(a,b)) ROS, (H) SOD, (I) LDH, and (J) MDA in cyst peripheral liver tissue in rat model infected with PSCs for 1 month; (K(a,b)) Western-blotting assay of Ferrostatin-1 on expression levels of ferroptosis signaling pathway proteins, such as TFRC, GPX4, FTH1, and SLC7A11, in liver tissues in rat model infected with PSCs for 1 month (n = 3 rats/group); * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 (Student t test).

Journal: Cells

Article Title: Echinococcus granulosus -Induced Liver Damage Through Ferroptosis in Rat Model.

doi: 10.3390/cells14050328

Figure Lengend Snippet: Figure 4. (A) Ferrostatin-1 inhibitor intervenes in vivo in PSC-mediated hepatocyte ferroptosis model establishment. (B) Characteristics of rat liver cyst morphology in rat blank control group, 1-month infection model group, and Ferrostatin-1 (5 mg/kg) intervention group. Cysts are indicated by white arrows (n = 6 rats/group). (C) Histological changes in Ferrostatin-1 on liver cysts in a rat model infected with PSCs for 1 month; germinal layer, keratinization layer, and inflammatory cell zone are indicated by black, white, and blue arrows (n = 6 rats/group; scale bars represent 100 µm and 50 µm). (D) TEM observation of Ferrostatin-1 on cyst peripheral hepatocyte ultra-structure changes in a rat model infected with PSCs for 1 month; mitochondria are indicated by white arrows (n = 3 rats/group; scale bars represent 2 µm and 1 µm). Effect of Ferrostatin-1 on (E) Fe2+, (F) GSH, (G(a,b)) ROS, (H) SOD, (I) LDH, and (J) MDA in cyst peripheral liver tissue in rat model infected with PSCs for 1 month; (K(a,b)) Western-blotting assay of Ferrostatin-1 on expression levels of ferroptosis signaling pathway proteins, such as TFRC, GPX4, FTH1, and SLC7A11, in liver tissues in rat model infected with PSCs for 1 month (n = 3 rats/group); * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 (Student t test).

Techniques: In Vivo, Control, Infection, Western Blot, Expressing

Figure 6. (A) Fe2+ in normal BRL cells, PSCs and BRL co-cultured cells, and PSCs +Ferrostatin-1 and BRL co-cultured cells. (B) GSH, (C) GSSH, (D) GSH/GSSH, (E) SOD, (F) LDH, and (G) MDA concentration detection (n = 6 rats/group). (H(a,b)) Western-blotting detection of expression levels of cell ferroptosis signaling pathway proteins in each group, such as TFRC, GPX4, FTH1, NOX1, SLC3A2, andSLC7A11 (n = 3 rats/group); * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 (Student t test).

Journal: Cells

Article Title: Echinococcus granulosus -Induced Liver Damage Through Ferroptosis in Rat Model.

doi: 10.3390/cells14050328

Figure Lengend Snippet: Figure 6. (A) Fe2+ in normal BRL cells, PSCs and BRL co-cultured cells, and PSCs +Ferrostatin-1 and BRL co-cultured cells. (B) GSH, (C) GSSH, (D) GSH/GSSH, (E) SOD, (F) LDH, and (G) MDA concentration detection (n = 6 rats/group). (H(a,b)) Western-blotting detection of expression levels of cell ferroptosis signaling pathway proteins in each group, such as TFRC, GPX4, FTH1, NOX1, SLC3A2, andSLC7A11 (n = 3 rats/group); * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 (Student t test).

Techniques: Cell Culture, Concentration Assay, Western Blot, Expressing

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