hy-n0890 Search Results


tbms1  (MedChemExpress)
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MedChemExpress tbms1
<t>TBMS1</t> inhibited the proliferation of HSFs. (A) IC 50 of TBMS1 for suppressing the proliferation of HSFs. (B) HSF viability following vehicle or TBMS1 treatment. (C) Cell morphology of HSFs following 48 h of treatment with vehicle or TBMS1 at various doses. (D) Flow cytometry and cell apoptosis analyses of HSFs treated with vehicle or TBMS1 (n = 3 separate assays). (E) Flow cytometry and cell cycle analyses of HSFs following treatment with vehicle or TBMS1 (n = 3 separate assays). (F) IC 50 of TBMS1 for suppressing NSF proliferation. (G) NSF viability was assessed following vehicle or TBMS1 treatment (4 μM) (n = 3 separate assays). The data suggest mean ± SD. Assay (B) was examined by one-way ANOVA with Tukey’s multiple comparison test, whereas assays (D) , (E) , and (F) were examined through unpaired two-tailed Student’s t tests; *P < 0.05, **P < 0.01, and ***P < 0.001.
Tbms1, 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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TBMS1 inhibited the proliferation of HSFs. (A) IC 50 of TBMS1 for suppressing the proliferation of HSFs. (B) HSF viability following vehicle or TBMS1 treatment. (C) Cell morphology of HSFs following 48 h of treatment with vehicle or TBMS1 at various doses. (D) Flow cytometry and cell apoptosis analyses of HSFs treated with vehicle or TBMS1 (n = 3 separate assays). (E) Flow cytometry and cell cycle analyses of HSFs following treatment with vehicle or TBMS1 (n = 3 separate assays). (F) IC 50 of TBMS1 for suppressing NSF proliferation. (G) NSF viability was assessed following vehicle or TBMS1 treatment (4 μM) (n = 3 separate assays). The data suggest mean ± SD. Assay (B) was examined by one-way ANOVA with Tukey’s multiple comparison test, whereas assays (D) , (E) , and (F) were examined through unpaired two-tailed Student’s t tests; *P < 0.05, **P < 0.01, and ***P < 0.001.

Journal: Frontiers in Pharmacology

Article Title: Targeted ferroptosis of myofibroblasts by tubeimoside I attenuates hypertrophic scar formation

doi: 10.3389/fphar.2025.1654108

Figure Lengend Snippet: TBMS1 inhibited the proliferation of HSFs. (A) IC 50 of TBMS1 for suppressing the proliferation of HSFs. (B) HSF viability following vehicle or TBMS1 treatment. (C) Cell morphology of HSFs following 48 h of treatment with vehicle or TBMS1 at various doses. (D) Flow cytometry and cell apoptosis analyses of HSFs treated with vehicle or TBMS1 (n = 3 separate assays). (E) Flow cytometry and cell cycle analyses of HSFs following treatment with vehicle or TBMS1 (n = 3 separate assays). (F) IC 50 of TBMS1 for suppressing NSF proliferation. (G) NSF viability was assessed following vehicle or TBMS1 treatment (4 μM) (n = 3 separate assays). The data suggest mean ± SD. Assay (B) was examined by one-way ANOVA with Tukey’s multiple comparison test, whereas assays (D) , (E) , and (F) were examined through unpaired two-tailed Student’s t tests; *P < 0.05, **P < 0.01, and ***P < 0.001.

Article Snippet: TBMS1 (MCE, HY-N0890), ferrostatin-1 (MCE, HY-100579), necrosulfonamide (MCE, HY-100573), 740Y-P (MCE, HY-P0175), Z-VAD-FMK (MCE, HY-16658B), Erastin (MCE, HY-15763) and ML385 (MCE, HY-100523) were used.

Techniques: Flow Cytometry, Comparison, Two Tailed Test

TBMS1 inhibited the migration of HSFs. (A) Images and Transwell assay quantitative analyses of the vehicle and TBMS1 groups (n = 5 separate assays); scale bar = 100 µm. (B) Images and wound healing quantitative analyses of the vehicle and TBMS1 groups (n = 3 separate assays). The scratch areas are represented by dotted lines; scale bar = 200 µm. (C) Western blotting was used for determining the MMP9 and MMP2 levels in vehicle-treated or TBMS1-treated HSFs. The data suggest mean ± SD. Experiments (A) , (B) , and (C) were examined through one-way ANOVA with Tukey’s multiple comparison test; *P < 0.05, **P < 0.01, and ***P < 0.001.

Journal: Frontiers in Pharmacology

Article Title: Targeted ferroptosis of myofibroblasts by tubeimoside I attenuates hypertrophic scar formation

doi: 10.3389/fphar.2025.1654108

Figure Lengend Snippet: TBMS1 inhibited the migration of HSFs. (A) Images and Transwell assay quantitative analyses of the vehicle and TBMS1 groups (n = 5 separate assays); scale bar = 100 µm. (B) Images and wound healing quantitative analyses of the vehicle and TBMS1 groups (n = 3 separate assays). The scratch areas are represented by dotted lines; scale bar = 200 µm. (C) Western blotting was used for determining the MMP9 and MMP2 levels in vehicle-treated or TBMS1-treated HSFs. The data suggest mean ± SD. Experiments (A) , (B) , and (C) were examined through one-way ANOVA with Tukey’s multiple comparison test; *P < 0.05, **P < 0.01, and ***P < 0.001.

Article Snippet: TBMS1 (MCE, HY-N0890), ferrostatin-1 (MCE, HY-100579), necrosulfonamide (MCE, HY-100573), 740Y-P (MCE, HY-P0175), Z-VAD-FMK (MCE, HY-16658B), Erastin (MCE, HY-15763) and ML385 (MCE, HY-100523) were used.

Techniques: Migration, Transwell Assay, Western Blot, Comparison

TBMS1 restrained HSF fibrotic phenotypes. (A) Representative images and collagen gel contraction quantitative analyses for the vehicle and TBMS1 groups (n = 3 separate assays). (B) Immunofluorescence analysis revealed α-SMA staining in vehicle-treated or TBMS1-treated HSFs; scale bar = 100 µm. (C–F) Western blotting was performed for determining COL I, COL III, and α-SMA contents of HSFs treated with vehicle or TBMS1. The data suggest mean ± SD. Experimental data (C–F) were examined via one-way ANOVA with Tukey’s multiple comparison test, whereas experimental data (A) were analyzed via an unpaired two-tailed Student’s t-test; *P < 0.05, **P < 0.01, and ***P < 0.001.

Journal: Frontiers in Pharmacology

Article Title: Targeted ferroptosis of myofibroblasts by tubeimoside I attenuates hypertrophic scar formation

doi: 10.3389/fphar.2025.1654108

Figure Lengend Snippet: TBMS1 restrained HSF fibrotic phenotypes. (A) Representative images and collagen gel contraction quantitative analyses for the vehicle and TBMS1 groups (n = 3 separate assays). (B) Immunofluorescence analysis revealed α-SMA staining in vehicle-treated or TBMS1-treated HSFs; scale bar = 100 µm. (C–F) Western blotting was performed for determining COL I, COL III, and α-SMA contents of HSFs treated with vehicle or TBMS1. The data suggest mean ± SD. Experimental data (C–F) were examined via one-way ANOVA with Tukey’s multiple comparison test, whereas experimental data (A) were analyzed via an unpaired two-tailed Student’s t-test; *P < 0.05, **P < 0.01, and ***P < 0.001.

Article Snippet: TBMS1 (MCE, HY-N0890), ferrostatin-1 (MCE, HY-100579), necrosulfonamide (MCE, HY-100573), 740Y-P (MCE, HY-P0175), Z-VAD-FMK (MCE, HY-16658B), Erastin (MCE, HY-15763) and ML385 (MCE, HY-100523) were used.

Techniques: Immunofluorescence, Staining, Western Blot, Comparison, Two Tailed Test

TBMS1 caused HSF ferroptosis. (A) The volcano plot displays significantly differentially-expressed genes (DEGs) in TBMS1-treated HSFs. (B) GSEA of DEGs in TBMS1-treated HSFs. Pathways related to PI3K/AKT pathway and ferroptosis are presented. (C) The heatmap shows typical TBMS1-regulated ferroptosis genes in HSFs. (D) The expression of the mRNAs of DEGs associated with ferroptosis in HSFs treated with vehicle or TBMS1 was estimated by qRT-PCR. (E) HSFs were treated with TBMS1 or TBMS1 combined with 1 µM ferrostatin-1, 10 µM Z-VAD-FMK, or 1 μM necrosulfonamide for 48 h before the measurement of cell viability (n = 3 separate assays). (F) ROS and MDA levels, intracellular Fe 2+ contents, and the GSH/GSSG ratio in vehicle-treated or TBMS1-treated HSFs (n = 3 separate assays). (G) ROS and MDA levels, intracellular Fe 2+ contents, and GSH/GSSG ratio of HSFs after treatment with TBMS1 or TBMS1 combined with ferrostatin-1 (1 µM) (n = 3 separate assays). (H) Western blotting illustrated TFR1 and DMT1 levels within HSFs after vehicle or TBMS1 treatment. (I) the Fe 2+ /Fe 3+ ratio in vehicle-treated or TBMS1-treated HSFs (n = 3 separate assays). (J) the Fe 2+ /Fe 3+ ratio of HSFs after treatment with TBMS1 or TBMS1 combined with ferrostatin-1 (1 µM) (n = 3 separate assays). The data suggest mean ± SD. Experiments (E–J) were examined via one-way ANOVA based on Tukey’s multiple comparison test, whereas assay (D) was performed via an unpaired two-tailed Student’s t-test; *P < 0.05, **P < 0.01, and ***P < 0.001.

Journal: Frontiers in Pharmacology

Article Title: Targeted ferroptosis of myofibroblasts by tubeimoside I attenuates hypertrophic scar formation

doi: 10.3389/fphar.2025.1654108

Figure Lengend Snippet: TBMS1 caused HSF ferroptosis. (A) The volcano plot displays significantly differentially-expressed genes (DEGs) in TBMS1-treated HSFs. (B) GSEA of DEGs in TBMS1-treated HSFs. Pathways related to PI3K/AKT pathway and ferroptosis are presented. (C) The heatmap shows typical TBMS1-regulated ferroptosis genes in HSFs. (D) The expression of the mRNAs of DEGs associated with ferroptosis in HSFs treated with vehicle or TBMS1 was estimated by qRT-PCR. (E) HSFs were treated with TBMS1 or TBMS1 combined with 1 µM ferrostatin-1, 10 µM Z-VAD-FMK, or 1 μM necrosulfonamide for 48 h before the measurement of cell viability (n = 3 separate assays). (F) ROS and MDA levels, intracellular Fe 2+ contents, and the GSH/GSSG ratio in vehicle-treated or TBMS1-treated HSFs (n = 3 separate assays). (G) ROS and MDA levels, intracellular Fe 2+ contents, and GSH/GSSG ratio of HSFs after treatment with TBMS1 or TBMS1 combined with ferrostatin-1 (1 µM) (n = 3 separate assays). (H) Western blotting illustrated TFR1 and DMT1 levels within HSFs after vehicle or TBMS1 treatment. (I) the Fe 2+ /Fe 3+ ratio in vehicle-treated or TBMS1-treated HSFs (n = 3 separate assays). (J) the Fe 2+ /Fe 3+ ratio of HSFs after treatment with TBMS1 or TBMS1 combined with ferrostatin-1 (1 µM) (n = 3 separate assays). The data suggest mean ± SD. Experiments (E–J) were examined via one-way ANOVA based on Tukey’s multiple comparison test, whereas assay (D) was performed via an unpaired two-tailed Student’s t-test; *P < 0.05, **P < 0.01, and ***P < 0.001.

Article Snippet: TBMS1 (MCE, HY-N0890), ferrostatin-1 (MCE, HY-100579), necrosulfonamide (MCE, HY-100573), 740Y-P (MCE, HY-P0175), Z-VAD-FMK (MCE, HY-16658B), Erastin (MCE, HY-15763) and ML385 (MCE, HY-100523) were used.

Techniques: Expressing, Quantitative RT-PCR, Western Blot, Comparison, Two Tailed Test

TBMS1 induced ferroptosis in HSFs by modulating PI3K/AKT pathway. (A) PI3K/AKT pathway levels in vehicle-treated or TBMS1-treated HSFs were detected by Western blotting. (B) Western blotting illustrated NRF2, SLC40A1, and GPX4 levels within HSFs after vehicle or TBMS1 treatment. (C) The p-AKT, NRF2, SLC40A1, and GPX4 protein levels in HSFs under TBMS1 or TBMS1 combined with 740Y-P (30 μM) treatment; 740Y-P is a PI3K/AKT pathway activator . (D) Cell viability under 48 h of treatment with TBMS1 or TBMS1 + 1 μM ferrostatin-1 (Fer-1) or 30 μM 740Y-P in HSFs (n = 3 separate assays). (E) COL I, COL III, and α-SMA proteins within HSFs treated with TBMS1 or TBMS1 combined with 740Y-P (30 μM). The data suggest mean ± SD. Assays (A–E) were examined based on one-way ANOVA with Tukey’s multiple comparison test; *P < 0.05, **P < 0.01, and ***P < 0.001.

Journal: Frontiers in Pharmacology

Article Title: Targeted ferroptosis of myofibroblasts by tubeimoside I attenuates hypertrophic scar formation

doi: 10.3389/fphar.2025.1654108

Figure Lengend Snippet: TBMS1 induced ferroptosis in HSFs by modulating PI3K/AKT pathway. (A) PI3K/AKT pathway levels in vehicle-treated or TBMS1-treated HSFs were detected by Western blotting. (B) Western blotting illustrated NRF2, SLC40A1, and GPX4 levels within HSFs after vehicle or TBMS1 treatment. (C) The p-AKT, NRF2, SLC40A1, and GPX4 protein levels in HSFs under TBMS1 or TBMS1 combined with 740Y-P (30 μM) treatment; 740Y-P is a PI3K/AKT pathway activator . (D) Cell viability under 48 h of treatment with TBMS1 or TBMS1 + 1 μM ferrostatin-1 (Fer-1) or 30 μM 740Y-P in HSFs (n = 3 separate assays). (E) COL I, COL III, and α-SMA proteins within HSFs treated with TBMS1 or TBMS1 combined with 740Y-P (30 μM). The data suggest mean ± SD. Assays (A–E) were examined based on one-way ANOVA with Tukey’s multiple comparison test; *P < 0.05, **P < 0.01, and ***P < 0.001.

Article Snippet: TBMS1 (MCE, HY-N0890), ferrostatin-1 (MCE, HY-100579), necrosulfonamide (MCE, HY-100573), 740Y-P (MCE, HY-P0175), Z-VAD-FMK (MCE, HY-16658B), Erastin (MCE, HY-15763) and ML385 (MCE, HY-100523) were used.

Techniques: Western Blot, Comparison

TBMS1 induced ferroptosis in HSFs by regulating NRF2/xCT/GPX4 pathway. (A) The x-CT, and GPX4 protein levels in HSFs under TBMS1 or TBMS1 combined with si-xCT treatment. (B) The x-CT, and GPX4 protein levels in HSFs under TBMS1 or TBMS1 combined with Erastin (5 μM) treatment. (C) The NRF2, and GPX4 protein levels in HSFs under TBMS1 or TBMS1 combined with ML385 (5 μM) treatment. The data suggest mean ± SD. Experiments (A–C) were examined via one-way ANOVA based on Tukey’s multiple comparison test; *P < 0.05, **P < 0.01, and ***P < 0.001.

Journal: Frontiers in Pharmacology

Article Title: Targeted ferroptosis of myofibroblasts by tubeimoside I attenuates hypertrophic scar formation

doi: 10.3389/fphar.2025.1654108

Figure Lengend Snippet: TBMS1 induced ferroptosis in HSFs by regulating NRF2/xCT/GPX4 pathway. (A) The x-CT, and GPX4 protein levels in HSFs under TBMS1 or TBMS1 combined with si-xCT treatment. (B) The x-CT, and GPX4 protein levels in HSFs under TBMS1 or TBMS1 combined with Erastin (5 μM) treatment. (C) The NRF2, and GPX4 protein levels in HSFs under TBMS1 or TBMS1 combined with ML385 (5 μM) treatment. The data suggest mean ± SD. Experiments (A–C) were examined via one-way ANOVA based on Tukey’s multiple comparison test; *P < 0.05, **P < 0.01, and ***P < 0.001.

Article Snippet: TBMS1 (MCE, HY-N0890), ferrostatin-1 (MCE, HY-100579), necrosulfonamide (MCE, HY-100573), 740Y-P (MCE, HY-P0175), Z-VAD-FMK (MCE, HY-16658B), Erastin (MCE, HY-15763) and ML385 (MCE, HY-100523) were used.

Techniques: Comparison

TBMS1 ameliorated rabbit ear HS formation. (A) The sketch map shows the rabbit ear HS model and TBMS1 treatments (40 and 400 μM). (B) Typical gross photographs show HS formation in rabbits. (C) Histological staining (H&E) and quantitative analysis of scar cross-sections of rabbit skin fibrotic tissues (n = 6 rabbits/group); scale bar = 200 μm. (D) Masson staining and quantitative analyses of rabbit scar SEIs (n = 6 rabbits/group). The long (D) and short (d) arrows represent the HS and neighboring unaffected skin tissue thicknesses, respectively. The “scar elevation index” was the D/d ratio; scale bar = 200 μm. (E) TGF-β1, COL I, COL III, and α-SMA mRNA expression within rabbit scar tissues following the administration of TBMS1 were measured via qRT-PCR (n = 3/group). (F) Representative images of immunohistochemical staining for CD31 in scar tissues from control group and TBMS1-treated group. Black arrows indicate blood vessels stained with an anti-CD31 antibody (n = 6 rabbits/group). scale bar = 100 μm. (G) The immunohistochemical staining for VEGF in scar tissues from control group and TBMS1-treated group (n = 6 rabbits/group). scale bar = 100 μm. The data suggest mean ± SD. Experiments (C–G) were assessed via one-way ANOVA with Tukey’s multiple comparison test; *P < 0.05, **P < 0.01, and ***P < 0.001.

Journal: Frontiers in Pharmacology

Article Title: Targeted ferroptosis of myofibroblasts by tubeimoside I attenuates hypertrophic scar formation

doi: 10.3389/fphar.2025.1654108

Figure Lengend Snippet: TBMS1 ameliorated rabbit ear HS formation. (A) The sketch map shows the rabbit ear HS model and TBMS1 treatments (40 and 400 μM). (B) Typical gross photographs show HS formation in rabbits. (C) Histological staining (H&E) and quantitative analysis of scar cross-sections of rabbit skin fibrotic tissues (n = 6 rabbits/group); scale bar = 200 μm. (D) Masson staining and quantitative analyses of rabbit scar SEIs (n = 6 rabbits/group). The long (D) and short (d) arrows represent the HS and neighboring unaffected skin tissue thicknesses, respectively. The “scar elevation index” was the D/d ratio; scale bar = 200 μm. (E) TGF-β1, COL I, COL III, and α-SMA mRNA expression within rabbit scar tissues following the administration of TBMS1 were measured via qRT-PCR (n = 3/group). (F) Representative images of immunohistochemical staining for CD31 in scar tissues from control group and TBMS1-treated group. Black arrows indicate blood vessels stained with an anti-CD31 antibody (n = 6 rabbits/group). scale bar = 100 μm. (G) The immunohistochemical staining for VEGF in scar tissues from control group and TBMS1-treated group (n = 6 rabbits/group). scale bar = 100 μm. The data suggest mean ± SD. Experiments (C–G) were assessed via one-way ANOVA with Tukey’s multiple comparison test; *P < 0.05, **P < 0.01, and ***P < 0.001.

Article Snippet: TBMS1 (MCE, HY-N0890), ferrostatin-1 (MCE, HY-100579), necrosulfonamide (MCE, HY-100573), 740Y-P (MCE, HY-P0175), Z-VAD-FMK (MCE, HY-16658B), Erastin (MCE, HY-15763) and ML385 (MCE, HY-100523) were used.

Techniques: Staining, Expressing, Quantitative RT-PCR, Immunohistochemical staining, Control, Comparison

The sketch map shows the molecular mechanism of TBMS1 in treating HS.

Journal: Frontiers in Pharmacology

Article Title: Targeted ferroptosis of myofibroblasts by tubeimoside I attenuates hypertrophic scar formation

doi: 10.3389/fphar.2025.1654108

Figure Lengend Snippet: The sketch map shows the molecular mechanism of TBMS1 in treating HS.

Article Snippet: TBMS1 (MCE, HY-N0890), ferrostatin-1 (MCE, HY-100579), necrosulfonamide (MCE, HY-100573), 740Y-P (MCE, HY-P0175), Z-VAD-FMK (MCE, HY-16658B), Erastin (MCE, HY-15763) and ML385 (MCE, HY-100523) were used.

Techniques: