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Structural and biological characterization of SIS and UBM-SIS meshes and isolated MBVs. A) Surface and cross-sectional morphology of SIS and UBM-SIS meshes by SEM. B) Quantification of mesh thickness (n = 10). C) Pore size and porosity analysis of mesh (n = 10). D) Live/dead staining of fibroblasts on SIS and UBM-SIS at day 1, 4, and 7. (E) CCK-8 assay of fibroblast viability on meshes (n = 5). F) Immunofluorescence staining of fibroblasts <t>(TGF-β1,</t> day 3), SMCs (phalloidin, day 7) and HUVECs (CD31, day 14) on SIS and UBM-SIS meshes, and SEM and DAPI staining of SMCs (day 21) coverage and cellular infiltration. White dashed lines delineate the upper and lower boundaries of the ECM scaffold. The yellow dashed line indicates the infiltration depth, defined as the distance from the scaffold surface to the DAPI-positive nucleus formed as a cellular floor and used for quantitative analysis. G) Quantification of TGF-β1, cytoskeletal area (phalloidin) and CD31 expression (n = 5). H) Quantification of cellular infiltration across mesh thickness (n = 5). I) Schematic of ECM components retained in decellularized ECM mesh. J) H&E and Masson's trichrome staining of mesh. K) Residual DNA quantification. L) Analysis of cytokine and growth factor profiling upon mesh-specific difference (n = 4). M) Workflow for MBV isolation and analysis. N) SEM images of MBV embedded on ECM. O) TEM images of MBV morphology. P) NTA analysis of MBV (n = 4). Q) Western blot detection of exosomal markers in MBV. Data are presented as mean ± SD. Each dot represents an independent sample. Statistical significance was determined using two-tailed unpaired Student's t-test for comparisons between two groups (B, C, and K), or one-way ANOVA followed by Tukey's post hoc test for multiple comparisons (E, G, and H), where ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001 and ∗∗∗∗ p < 0.0001.

Tgf β1, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 96/100, based on 1477 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/tgf+%CE%B21/TGF%CE%B21/pmc13020019-427-7-24
Average 96 stars, based on 1477 article reviews

tgf β1 - by Bioz Stars, 2026-09

96/100 stars

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1) Product Images from "Tissue-specific matrix-bound nanovesicles regulate the immunoregulatory progress of biological mesh-aided abdominal hernia repair"

Article Title: Tissue-specific matrix-bound nanovesicles regulate the immunoregulatory progress of biological mesh-aided abdominal hernia repair

Journal: Bioactive Materials

doi: 10.1016/j.bioactmat.2026.03.004

Figure Legend Snippet: Structural and biological characterization of SIS and UBM-SIS meshes and isolated MBVs. A) Surface and cross-sectional morphology of SIS and UBM-SIS meshes by SEM. B) Quantification of mesh thickness (n = 10). C) Pore size and porosity analysis of mesh (n = 10). D) Live/dead staining of fibroblasts on SIS and UBM-SIS at day 1, 4, and 7. (E) CCK-8 assay of fibroblast viability on meshes (n = 5). F) Immunofluorescence staining of fibroblasts (TGF-β1, day 3), SMCs (phalloidin, day 7) and HUVECs (CD31, day 14) on SIS and UBM-SIS meshes, and SEM and DAPI staining of SMCs (day 21) coverage and cellular infiltration. White dashed lines delineate the upper and lower boundaries of the ECM scaffold. The yellow dashed line indicates the infiltration depth, defined as the distance from the scaffold surface to the DAPI-positive nucleus formed as a cellular floor and used for quantitative analysis. G) Quantification of TGF-β1, cytoskeletal area (phalloidin) and CD31 expression (n = 5). H) Quantification of cellular infiltration across mesh thickness (n = 5). I) Schematic of ECM components retained in decellularized ECM mesh. J) H&E and Masson's trichrome staining of mesh. K) Residual DNA quantification. L) Analysis of cytokine and growth factor profiling upon mesh-specific difference (n = 4). M) Workflow for MBV isolation and analysis. N) SEM images of MBV embedded on ECM. O) TEM images of MBV morphology. P) NTA analysis of MBV (n = 4). Q) Western blot detection of exosomal markers in MBV. Data are presented as mean ± SD. Each dot represents an independent sample. Statistical significance was determined using two-tailed unpaired Student's t-test for comparisons between two groups (B, C, and K), or one-way ANOVA followed by Tukey's post hoc test for multiple comparisons (E, G, and H), where ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001 and ∗∗∗∗ p < 0.0001.

Techniques Used: Isolation, Pore Size, Staining, CCK-8 Assay, Immunofluorescence, Expressing, Western Blot, Two Tailed Test

Bioactivity and immunomodulatory properties of MBVs derived from SIS and UBM-SIS meshes. A) Schematic illustration of MBV-regulated cellular activities during ECM remodeling via their interactions with fibroblasts, SMCs, HUVECs, and macrophages to validate MBVs as bioactive components embedded within parent ECM. Nuclei are labeled with DAPI (blue); PKH26 (red) marks MBVs; phalloidin (green) stains F-actin. B) Immunofluorescence staining of fibroblasts (TGF-β1, collagen I), SMCs (phalloidin), and HUVECs (CD31) after treatment with SIS MBVs or UBM-SIS MBVs. C) Quantification of fluorescence signal area per cell for respective markers (n = 5). D) Western blot analysis of marker proteins in MBV-treated cells. E) Relative protein expression levels normalized to GAPDH (n = 3). F) Schematic of macrophage polarization model with/without MBV treatment. G) Immunostaining of macrophages for F4/80, iNOS (M1-like), and Arg-1 (M2-like) under different stimulations and MBV-treated conditions. H) Quantification of mean fluorescence intensity (MFI) of iNOS and Arg-1 (n = 5). I) Western blot analysis of pro- and anti-inflammatory markers in MBV-treated macrophages and LPS + IFN-γ-treated macrophages (control). J) Quantification of relative protein levels (n = 3). K) Heatmap of RT-qPCR analysis showing cytokine and ECM regulator gene expression in MBV-treated macrophages (n = 3). L) Representative fluorescence images of DCFH staining in macrophages following different treatments. M) Quantification of DCFH fluorescence area per cell (n = 5). Data are presented as mean ± SD. Each dot represents an independent biological replicate. Statistical significance was assessed using one-way ANOVA followed by Tukey's post hoc test, where ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001 and ∗∗∗∗ p < 0.0001.

Figure Legend Snippet: Bioactivity and immunomodulatory properties of MBVs derived from SIS and UBM-SIS meshes. A) Schematic illustration of MBV-regulated cellular activities during ECM remodeling via their interactions with fibroblasts, SMCs, HUVECs, and macrophages to validate MBVs as bioactive components embedded within parent ECM. Nuclei are labeled with DAPI (blue); PKH26 (red) marks MBVs; phalloidin (green) stains F-actin. B) Immunofluorescence staining of fibroblasts (TGF-β1, collagen I), SMCs (phalloidin), and HUVECs (CD31) after treatment with SIS MBVs or UBM-SIS MBVs. C) Quantification of fluorescence signal area per cell for respective markers (n = 5). D) Western blot analysis of marker proteins in MBV-treated cells. E) Relative protein expression levels normalized to GAPDH (n = 3). F) Schematic of macrophage polarization model with/without MBV treatment. G) Immunostaining of macrophages for F4/80, iNOS (M1-like), and Arg-1 (M2-like) under different stimulations and MBV-treated conditions. H) Quantification of mean fluorescence intensity (MFI) of iNOS and Arg-1 (n = 5). I) Western blot analysis of pro- and anti-inflammatory markers in MBV-treated macrophages and LPS + IFN-γ-treated macrophages (control). J) Quantification of relative protein levels (n = 3). K) Heatmap of RT-qPCR analysis showing cytokine and ECM regulator gene expression in MBV-treated macrophages (n = 3). L) Representative fluorescence images of DCFH staining in macrophages following different treatments. M) Quantification of DCFH fluorescence area per cell (n = 5). Data are presented as mean ± SD. Each dot represents an independent biological replicate. Statistical significance was assessed using one-way ANOVA followed by Tukey's post hoc test, where ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001 and ∗∗∗∗ p < 0.0001.

Techniques Used: Derivative Assay, Labeling, Immunofluorescence, Staining, Fluorescence, Western Blot, Marker, Expressing, Immunostaining, Control, Quantitative RT-PCR, Gene Expression

Functional comparison of MBVs derived from SIS and UBM in modulating inflammation, angiogenesis, and matrix remodeling. A) Schematic of macrophage polarization model under LPS + IFN-γ stimulation with or without MBV treatment. B) Immunofluorescence staining of iNOS (red) and Arg-1 (green) in macrophages treated with SIS MBVs, UBM MBVs, or UBM-SIS MBVs. C) Quantification of mean fluorescence intensity (MFI) of iNOS and Arg-1 (n = 5). D–G) RT-qPCR analysis of pro- (( TNF-α, IL-6 ) and anti-inflammatory ( IL-10, TGF-β1 ) cytokine gene expression in MBV-treated macrophages (n = 4). H) Schematic of analysis of MBV-treated HUVECs and fibroblasts cultured in Matrigel. I) 3D immunostaining of CD31 + tube-like structures in HUVECs after MBV treatment. J–K) Quantification of tube-like area percentage and number of tube-like structures per field (n = 6). L) 3D two-photo images of TGF-β1 expression in fibroblasts cultured with different MBVs. M) Quantification of TGF-β1-positive volume percentage in fibroblasts (n = 4). N-P) Western blot analysis of NF-κB and STAT3 pathway proteins in MBV-treated macrophages, angiogenic signaling proteins (AKT, ERK1/2) in MBV-treated HUVECs, TGF-β/Smad signaling pathway in MBV-treated fibroblasts. Quantification of respective signaling molecules (n = 3). Data are presented as mean ± SD. Each dot represents an independent biological replicate. Statistical significance was assessed using one-way ANOVA followed by Tukey's post hoc test for multiple comparisons, where ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001.

Figure Legend Snippet: Functional comparison of MBVs derived from SIS and UBM in modulating inflammation, angiogenesis, and matrix remodeling. A) Schematic of macrophage polarization model under LPS + IFN-γ stimulation with or without MBV treatment. B) Immunofluorescence staining of iNOS (red) and Arg-1 (green) in macrophages treated with SIS MBVs, UBM MBVs, or UBM-SIS MBVs. C) Quantification of mean fluorescence intensity (MFI) of iNOS and Arg-1 (n = 5). D–G) RT-qPCR analysis of pro- (( TNF-α, IL-6 ) and anti-inflammatory ( IL-10, TGF-β1 ) cytokine gene expression in MBV-treated macrophages (n = 4). H) Schematic of analysis of MBV-treated HUVECs and fibroblasts cultured in Matrigel. I) 3D immunostaining of CD31 + tube-like structures in HUVECs after MBV treatment. J–K) Quantification of tube-like area percentage and number of tube-like structures per field (n = 6). L) 3D two-photo images of TGF-β1 expression in fibroblasts cultured with different MBVs. M) Quantification of TGF-β1-positive volume percentage in fibroblasts (n = 4). N-P) Western blot analysis of NF-κB and STAT3 pathway proteins in MBV-treated macrophages, angiogenic signaling proteins (AKT, ERK1/2) in MBV-treated HUVECs, TGF-β/Smad signaling pathway in MBV-treated fibroblasts. Quantification of respective signaling molecules (n = 3). Data are presented as mean ± SD. Each dot represents an independent biological replicate. Statistical significance was assessed using one-way ANOVA followed by Tukey's post hoc test for multiple comparisons, where ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001.

Techniques Used: Functional Assay, Comparison, Derivative Assay, Immunofluorescence, Staining, Fluorescence, Quantitative RT-PCR, Gene Expression, Cell Culture, Immunostaining, Expressing, Western Blot

Inflammatory immune responses following mesh implantation. A) Schematic illustration and representative macroscopic images of seroma tissues collected from the explants at 1 week. B) ELISA analysis of cytokines in the seroma fluid after 1 week (n = 4). C) Representative immunofluorescence images of CD11b + cell infiltration in mesh at 1 and 4 weeks. Scale bars: left, 1000 μm; right, 50 μm. D–E) Quantification of CD11b + cell density (n = 5, 4 samples per rat). F) Representative immunofluorescence images of CD68 (yellow), CD86 (green), and CD206 (red) staining of SIS and UBM-SIS at 1 and 4 weeks. Scale bars: top, 1000 μm; bottom, 50 μm. G–H) Quantification of CD68 + macrophage infiltration and M2-like/M1-like phenotypic distribution at 1 week (n = 5). I) Statistical comparison of M2-like/M1-like ratios between SIS and UBM-SIS groups (n = 5). J–K) CD68 + macrophage infiltration and CD206 + /CD86 + phenotypic distribution at 4 weeks (n = 5, 4 samples per rat). L) Quantification of M2-like/M1-like ratios at 4 weeks (n = 5, 4 samples per rat). M−O) Representative immunofluorescence images of iNOS and Arg-1 at tissue-mesh interfaces at 1 and 4 weeks, with quantitative analysis of positive area (n = 5, with 4 samples per rat). Scale bars: 50 μm. P) RT-qPCR analysis of pro- (( TNF-α, IL-6 ) and anti-inflammatory ( IL-10, TGF-β1 ) cytokine gene expression in SIS and UBM-SIS explants. Q) Schematic summary of immune response transition induced by SIS versus UBM-SIS MBV-containing meshes over 4 weeks. The asterisk indicates the implanted mesh. Data are presented as mean ± SD. For (B, I, L, and P), mean value of each rat (n = 5) was used for statistical comparisons. For (D, E, G, H, J, K, N, and O), each dot represents one section-level sample, where the value of each animal for statistical comparisons was obtained by averaging measurements from 4 samples. Statistical comparisons were performed within each time point using two-tailed unpaired Student's t-test, where ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001.

Figure Legend Snippet: Inflammatory immune responses following mesh implantation. A) Schematic illustration and representative macroscopic images of seroma tissues collected from the explants at 1 week. B) ELISA analysis of cytokines in the seroma fluid after 1 week (n = 4). C) Representative immunofluorescence images of CD11b + cell infiltration in mesh at 1 and 4 weeks. Scale bars: left, 1000 μm; right, 50 μm. D–E) Quantification of CD11b + cell density (n = 5, 4 samples per rat). F) Representative immunofluorescence images of CD68 (yellow), CD86 (green), and CD206 (red) staining of SIS and UBM-SIS at 1 and 4 weeks. Scale bars: top, 1000 μm; bottom, 50 μm. G–H) Quantification of CD68 + macrophage infiltration and M2-like/M1-like phenotypic distribution at 1 week (n = 5). I) Statistical comparison of M2-like/M1-like ratios between SIS and UBM-SIS groups (n = 5). J–K) CD68 + macrophage infiltration and CD206 + /CD86 + phenotypic distribution at 4 weeks (n = 5, 4 samples per rat). L) Quantification of M2-like/M1-like ratios at 4 weeks (n = 5, 4 samples per rat). M−O) Representative immunofluorescence images of iNOS and Arg-1 at tissue-mesh interfaces at 1 and 4 weeks, with quantitative analysis of positive area (n = 5, with 4 samples per rat). Scale bars: 50 μm. P) RT-qPCR analysis of pro- (( TNF-α, IL-6 ) and anti-inflammatory ( IL-10, TGF-β1 ) cytokine gene expression in SIS and UBM-SIS explants. Q) Schematic summary of immune response transition induced by SIS versus UBM-SIS MBV-containing meshes over 4 weeks. The asterisk indicates the implanted mesh. Data are presented as mean ± SD. For (B, I, L, and P), mean value of each rat (n = 5) was used for statistical comparisons. For (D, E, G, H, J, K, N, and O), each dot represents one section-level sample, where the value of each animal for statistical comparisons was obtained by averaging measurements from 4 samples. Statistical comparisons were performed within each time point using two-tailed unpaired Student's t-test, where ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001.

Techniques Used: Enzyme-linked Immunosorbent Assay, Immunofluorescence, Staining, Comparison, Quantitative RT-PCR, Gene Expression, Two Tailed Test

ECM remodeling and mechanical evaluation of meshes and explants. A) Representative immunofluorescence images showing collagen I (red) and collagen III (green) deposition in the center and interface regions of SIS and UBM–SIS explants at 8 weeks. Scale bars: overview = 1000 μm, magnified images = 100 μm. B–E) Quantification of total collagen (I + III), collagen I, and collagen III positive expression and collagen I/III ratio in the center and interface regions (n = 5, 4 samples per rat). F–G) Polar plot of collagen fiber orientation in the center and interface regions analyzed by orientation distribution. H) Orientation coherency of collagen fibers in the center and interface regions (n = 5, 4 samples per rat). I) Aspect ratio analysis indicating collagen fibril anisotropy (n = 4). J–K) Representative immunofluorescence staining of TGF-β1 and α-SMA at 8 weeks and corresponding quantification of positive area (n = 5, 4 samples per rat). L, M) Mechanical characterization of meshes and explants showing ultimate tensile strength and elongation at break across different time points (n = 4). N) Comparison of tensile strength and elongation of explants with native abdominal wall components, including posterior and anterior rectus sheath, linea alba, peritoneum, and transversalis fascia. The asterisk indicates the implanted mesh. Data are presented as mean ± SD. For (B-E, H, and K), mean value of each rat (n = 5) was used for statistical comparisons. Each dot represents one section-level sample, where the value for each animal was obtained by averaging measurements from 4 samples. For (I, L, and M), mean value of each rat (n = 4) was used for statistical comparisons. Statistical significance was determined using two-tailed unpaired Student's t-test, where ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001.

Figure Legend Snippet: ECM remodeling and mechanical evaluation of meshes and explants. A) Representative immunofluorescence images showing collagen I (red) and collagen III (green) deposition in the center and interface regions of SIS and UBM–SIS explants at 8 weeks. Scale bars: overview = 1000 μm, magnified images = 100 μm. B–E) Quantification of total collagen (I + III), collagen I, and collagen III positive expression and collagen I/III ratio in the center and interface regions (n = 5, 4 samples per rat). F–G) Polar plot of collagen fiber orientation in the center and interface regions analyzed by orientation distribution. H) Orientation coherency of collagen fibers in the center and interface regions (n = 5, 4 samples per rat). I) Aspect ratio analysis indicating collagen fibril anisotropy (n = 4). J–K) Representative immunofluorescence staining of TGF-β1 and α-SMA at 8 weeks and corresponding quantification of positive area (n = 5, 4 samples per rat). L, M) Mechanical characterization of meshes and explants showing ultimate tensile strength and elongation at break across different time points (n = 4). N) Comparison of tensile strength and elongation of explants with native abdominal wall components, including posterior and anterior rectus sheath, linea alba, peritoneum, and transversalis fascia. The asterisk indicates the implanted mesh. Data are presented as mean ± SD. For (B-E, H, and K), mean value of each rat (n = 5) was used for statistical comparisons. Each dot represents one section-level sample, where the value for each animal was obtained by averaging measurements from 4 samples. For (I, L, and M), mean value of each rat (n = 4) was used for statistical comparisons. Statistical significance was determined using two-tailed unpaired Student's t-test, where ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001.

Techniques Used: Immunofluorescence, Expressing, Staining, Comparison, Two Tailed Test

Transcriptomic analysis of explants from different groups after 1 week and comparative analysis of MBV and ECM properties. A) Schematic illustration of tissues collected from the explants at 1 week for distinct signaling pathway analysis. B) Volcano plot showing differentially expressed genes (DEGs) between UBM-SIS and SIS groups (n = 3 per group). C) Heatmap of DEGs between SIS and UBM-SIS groups (red: upregulated, blue: downregulated; cutoff >1.0; n = 3). D) KEGG pathway enrichment analysis of downregulated genes in UBM-SIS compared to SIS. E) Reactome pathway enrichment analysis of downregulated genes in UBM-SIS compared to SIS. F–H) GSEA demonstrating altered gene signatures related to NET formation, NF-κB pathway and cytokine-cytokine receptor interaction. I) Radar plot comparing SIS- and UBM-derived MBVs. The five axes represent key pathways involved in angiogenesis ( ERK ), vascularization ( AKT ), inflammation ( p65 ), immunomodulation ( STAT3 ), and remodeling ( TGF-β/Smad ). J) Radar plot summarizing ECM in vivo performance at 1 and 4 weeks. The five axes represent essential features in ECM remodeling, including adhesion, angiogenesis, inflammation, immunomodulation, and collagen deposition.

Figure Legend Snippet: Transcriptomic analysis of explants from different groups after 1 week and comparative analysis of MBV and ECM properties. A) Schematic illustration of tissues collected from the explants at 1 week for distinct signaling pathway analysis. B) Volcano plot showing differentially expressed genes (DEGs) between UBM-SIS and SIS groups (n = 3 per group). C) Heatmap of DEGs between SIS and UBM-SIS groups (red: upregulated, blue: downregulated; cutoff >1.0; n = 3). D) KEGG pathway enrichment analysis of downregulated genes in UBM-SIS compared to SIS. E) Reactome pathway enrichment analysis of downregulated genes in UBM-SIS compared to SIS. F–H) GSEA demonstrating altered gene signatures related to NET formation, NF-κB pathway and cytokine-cytokine receptor interaction. I) Radar plot comparing SIS- and UBM-derived MBVs. The five axes represent key pathways involved in angiogenesis ( ERK ), vascularization ( AKT ), inflammation ( p65 ), immunomodulation ( STAT3 ), and remodeling ( TGF-β/Smad ). J) Radar plot summarizing ECM in vivo performance at 1 and 4 weeks. The five axes represent essential features in ECM remodeling, including adhesion, angiogenesis, inflammation, immunomodulation, and collagen deposition.

Techniques Used: Derivative Assay, In Vivo

Incubation:

Article Title: Dual knockdown of Alox15 and TGF-β1 by lipid nanoparticle-delivered siRNA in bleomycin-induced pulmonary fibrosis
Article Snippet: .. The membranes were then incubated overnight at 4 °C with primary antibodies against Alox15 (ab244205, Abcam), 4-HNE (ab48506, Abcam), TGF-β1 (sc-130348, Santa Cruz Biotechnology, USA), E-cadherin (IR55-180, iReal Biotechnology), Vimentin (GTX100619, GeneTex, Taiwan), α-SMA (E-AB-34268, Elabscience, China), or GAPDH (2118, Cell Signaling Technology, Danvers, MA, USA). ..

Article Title: Chronic ACL Injury Drives a Fibrotic and Matrix-Degradative Shift: A Multi-Level Analysis of MMP-13 and TGF-β1.
Article Snippet: .. Sections were incubated overnight at 4 ◦C with primary antibodies against MMP-13 (sc-515284, 1:100 dilution) and TGF-β1 (sc-130348, 1:100 dilution) obtained from Santa Cruz Biotechnology (Dallas, TX, USA). .. The next day, the slides were incubated with a biotinylated secondary antibody and visualized using a DAB (3,3′-diaminobenzidine, TA-125-HDX, Thermo Fisher Scientific, Waltham, MA, USA) substrate kit.

Article Title: Chronic ACL Injury Drives a Fibrotic and Matrix-Degradative Shift: A Multi-Level Analysis of MMP-13 and TGF-β1
Article Snippet: .. Sections were incubated overnight at 4 °C with primary antibodies against MMP-13 (sc-515284, 1:100 dilution) and TGF-β1 (sc-130348, 1:100 dilution) obtained from Santa Cruz Biotechnology (Dallas, TX, USA). .. The next day, the slides were incubated with a biotinylated secondary antibody and visualized using a DAB (3,3′-diaminobenzidine, TA-125-HDX, Thermo Fisher Scientific, Waltham, MA, USA) substrate kit.

Article Title: Zingiber zerumbet rhizome attenuates bleomycin-induced pulmonary fibrosis by regulating TGF-β1 and TNF/NF-κB signaling to inhibit epithelial-mesenchymal transition and fibroblast activation.
Article Snippet: Ethnopharmacological relevance: Zingiber zerumbet (L.) Smith rhizome has long been employed in traditional medicine across Asia for managing respiratory disorders, suggesting its potential utility in chronic fibrotic lung

Article Title: Cannabis oil modulates liver alterations and endocannabinoid system changes in a female rat model of diet-induced MASLD
Article Snippet: The sections were mounted on 3-aminopropyltriethoxysilane (Sigma-Aldrich, Buenos Aires, Argentine)-coated slides and a subsequent microwave pretreatment for antigen retrieval was performed. .. The samples were incubated in a humid chamber first with a specific primary antibody for 4-HNE (mouse monoclonal antibody; Catalog # MAB3249; R&D Systems), NrF2 (mouse monoclonal antibody; sc-365949; Santa Cruz Biotechnology), NF-κB p65 (mouse monoclonal antibody; sc-8008; Santa Cruz Biotechnology) and TGF-β1 (mouse monoclonal antibody; sc-52893; Santa Cruz Biotechnology) (for 14–16 h at 4°C) and then with biotin-conjugated secondary antibody (anti-mouse, 1:100 dilution, Sigma) for 30 min at room temperature. .. The reactions were developed using the streptavidin–biotin peroxidase method and diaminobenzidine (Sigma) as a chromogenic substrate.

Bicinchoninic Acid Protein Assay:

Article Title: Tissue-specific matrix-bound nanovesicles regulate the immunoregulatory progress of biological mesh-aided abdominal hernia repair
Article Snippet: Primary antibodies, including rabbit anti-CD63, CD81, CD9, and HSP70, and anti -F4/80, iNOS, Arg-1, p-ERK1/2, TNF-α, IL-10 were purchased from Abcam (Cambridge, MA, USA). .. Additional antibodies, such as mouse polyclonal anti -TGF-β1, anti-elastin, CD11b, CD68, CD86, and CD206, along with the BCA Protein Assay Kit, were obtained from Santa Cruz Biotechnology (Dallas, TX, USA). ..

Immunofluorescence:

Article Title: Nanoparticle IL-33 Covalent Pericardial Patch Inhibits Pseudoaneurysm Formation after Aortic Patch Angioplasty.
Article Snippet: Background: Pseudoaneurysm is a complication of interventional surgery and other vascular injuries; the formation mechanism is unclear.. The purpose of this study was to explore the mechanism of IL-33 in pseudoaneurysms and develop a pericardial patch coated with IL-33 PLGA nanoparticles to inhibit pseudoaneurysm formation Methods: Rats were sacrificed on day 30 to observe the formation of pseudoaneurysms in NP-IL-33, NP-TGFβ-coated, and control groups.. Histological staining was used to evaluate the size and breakage of the elastic fibers.

Immunohistochemical staining:

Article Title: Time-dependent effects of topical mucopolysaccharide polysulfate and silver sulfadiazine on wound healing in a rat excisional wound model.
Article Snippet: .. [12] To evaluate the molecular involvement in wound healing, immunohistochemical staining for TGF-β1 (Santa Cruz Biotechnology, dilution 1:100) was performed on paraffin-embedded tissue sections (Figure 4). ..

Staining:

Image Search Results

Journal: Bioactive Materials

Article Title: Mesenchymal stromal cells-loaded 3D radially aligned composite scaffold with potentiated paracrine signaling for sequential bone regeneration

doi: 10.1016/j.bioactmat.2026.02.059

Figure Lengend Snippet: Temporal analysis of the BMSC paracrine profile on different scaffolds. (A) Confocal microscopy images from Live/Dead fluorescence staining of BMSCs encapsulated within the PCL/HAp-GelMA/BMSCs scaffold after 1, 3, 5, and 14 d of 3D culture (live cells, green; dead cells, red). (B) The concentrations of key paracrine factors (TGF-β, PGE2, VEGF, HGF, and BMP-2) from BMSCs cultured in different scaffolds, quantified from culture supernatants at day 3 and day 7. (C) Corresponding relative mRNA expression levels of TGFB1, PTGS2, VEGFA, HGF, and BMP-2 in BMSCs at day 3 and day 7, as determined by qPCR analysis. Data are presented as mean ± SD (n = 3) *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001; ns: not significant.

Article Snippet: ELISA kits for PGE2 (Cat. No. E-EL-0034), TGF-β (Cat. No. E-EL-0162), VEGF (Cat. No. E-EL-R2603), and HGF (Cat. No. E-EL-R0496) were purchased from Elabscience (Wuhan, China).

Techniques: Confocal Microscopy, Fluorescence, Staining, Cell Culture, Expressing

Journal: Bioactive Materials

Article Title: Tissue-specific matrix-bound nanovesicles regulate the immunoregulatory progress of biological mesh-aided abdominal hernia repair

doi: 10.1016/j.bioactmat.2026.03.004

Figure Lengend Snippet: Structural and biological characterization of SIS and UBM-SIS meshes and isolated MBVs. A) Surface and cross-sectional morphology of SIS and UBM-SIS meshes by SEM. B) Quantification of mesh thickness (n = 10). C) Pore size and porosity analysis of mesh (n = 10). D) Live/dead staining of fibroblasts on SIS and UBM-SIS at day 1, 4, and 7. (E) CCK-8 assay of fibroblast viability on meshes (n = 5). F) Immunofluorescence staining of fibroblasts (TGF-β1, day 3), SMCs (phalloidin, day 7) and HUVECs (CD31, day 14) on SIS and UBM-SIS meshes, and SEM and DAPI staining of SMCs (day 21) coverage and cellular infiltration. White dashed lines delineate the upper and lower boundaries of the ECM scaffold. The yellow dashed line indicates the infiltration depth, defined as the distance from the scaffold surface to the DAPI-positive nucleus formed as a cellular floor and used for quantitative analysis. G) Quantification of TGF-β1, cytoskeletal area (phalloidin) and CD31 expression (n = 5). H) Quantification of cellular infiltration across mesh thickness (n = 5). I) Schematic of ECM components retained in decellularized ECM mesh. J) H&E and Masson's trichrome staining of mesh. K) Residual DNA quantification. L) Analysis of cytokine and growth factor profiling upon mesh-specific difference (n = 4). M) Workflow for MBV isolation and analysis. N) SEM images of MBV embedded on ECM. O) TEM images of MBV morphology. P) NTA analysis of MBV (n = 4). Q) Western blot detection of exosomal markers in MBV. Data are presented as mean ± SD. Each dot represents an independent sample. Statistical significance was determined using two-tailed unpaired Student's t-test for comparisons between two groups (B, C, and K), or one-way ANOVA followed by Tukey's post hoc test for multiple comparisons (E, G, and H), where ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001 and ∗∗∗∗ p < 0.0001.

Article Snippet: Additional antibodies, such as mouse polyclonal anti -TGF-β1, anti-elastin, CD11b, CD68, CD86, and CD206, along with the BCA Protein Assay Kit, were obtained from Santa Cruz Biotechnology (Dallas, TX, USA).

Techniques: Isolation, Pore Size, Staining, CCK-8 Assay, Immunofluorescence, Expressing, Western Blot, Two Tailed Test

Journal: Bioactive Materials

Article Title: Tissue-specific matrix-bound nanovesicles regulate the immunoregulatory progress of biological mesh-aided abdominal hernia repair

doi: 10.1016/j.bioactmat.2026.03.004

Figure Lengend Snippet: Bioactivity and immunomodulatory properties of MBVs derived from SIS and UBM-SIS meshes. A) Schematic illustration of MBV-regulated cellular activities during ECM remodeling via their interactions with fibroblasts, SMCs, HUVECs, and macrophages to validate MBVs as bioactive components embedded within parent ECM. Nuclei are labeled with DAPI (blue); PKH26 (red) marks MBVs; phalloidin (green) stains F-actin. B) Immunofluorescence staining of fibroblasts (TGF-β1, collagen I), SMCs (phalloidin), and HUVECs (CD31) after treatment with SIS MBVs or UBM-SIS MBVs. C) Quantification of fluorescence signal area per cell for respective markers (n = 5). D) Western blot analysis of marker proteins in MBV-treated cells. E) Relative protein expression levels normalized to GAPDH (n = 3). F) Schematic of macrophage polarization model with/without MBV treatment. G) Immunostaining of macrophages for F4/80, iNOS (M1-like), and Arg-1 (M2-like) under different stimulations and MBV-treated conditions. H) Quantification of mean fluorescence intensity (MFI) of iNOS and Arg-1 (n = 5). I) Western blot analysis of pro- and anti-inflammatory markers in MBV-treated macrophages and LPS + IFN-γ-treated macrophages (control). J) Quantification of relative protein levels (n = 3). K) Heatmap of RT-qPCR analysis showing cytokine and ECM regulator gene expression in MBV-treated macrophages (n = 3). L) Representative fluorescence images of DCFH staining in macrophages following different treatments. M) Quantification of DCFH fluorescence area per cell (n = 5). Data are presented as mean ± SD. Each dot represents an independent biological replicate. Statistical significance was assessed using one-way ANOVA followed by Tukey's post hoc test, where ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001 and ∗∗∗∗ p < 0.0001.

Techniques: Derivative Assay, Labeling, Immunofluorescence, Staining, Fluorescence, Western Blot, Marker, Expressing, Immunostaining, Control, Quantitative RT-PCR, Gene Expression

Journal: Bioactive Materials

Article Title: Tissue-specific matrix-bound nanovesicles regulate the immunoregulatory progress of biological mesh-aided abdominal hernia repair

doi: 10.1016/j.bioactmat.2026.03.004

Figure Lengend Snippet: Functional comparison of MBVs derived from SIS and UBM in modulating inflammation, angiogenesis, and matrix remodeling. A) Schematic of macrophage polarization model under LPS + IFN-γ stimulation with or without MBV treatment. B) Immunofluorescence staining of iNOS (red) and Arg-1 (green) in macrophages treated with SIS MBVs, UBM MBVs, or UBM-SIS MBVs. C) Quantification of mean fluorescence intensity (MFI) of iNOS and Arg-1 (n = 5). D–G) RT-qPCR analysis of pro- (( TNF-α, IL-6 ) and anti-inflammatory ( IL-10, TGF-β1 ) cytokine gene expression in MBV-treated macrophages (n = 4). H) Schematic of analysis of MBV-treated HUVECs and fibroblasts cultured in Matrigel. I) 3D immunostaining of CD31 + tube-like structures in HUVECs after MBV treatment. J–K) Quantification of tube-like area percentage and number of tube-like structures per field (n = 6). L) 3D two-photo images of TGF-β1 expression in fibroblasts cultured with different MBVs. M) Quantification of TGF-β1-positive volume percentage in fibroblasts (n = 4). N-P) Western blot analysis of NF-κB and STAT3 pathway proteins in MBV-treated macrophages, angiogenic signaling proteins (AKT, ERK1/2) in MBV-treated HUVECs, TGF-β/Smad signaling pathway in MBV-treated fibroblasts. Quantification of respective signaling molecules (n = 3). Data are presented as mean ± SD. Each dot represents an independent biological replicate. Statistical significance was assessed using one-way ANOVA followed by Tukey's post hoc test for multiple comparisons, where ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001.

Techniques: Functional Assay, Comparison, Derivative Assay, Immunofluorescence, Staining, Fluorescence, Quantitative RT-PCR, Gene Expression, Cell Culture, Immunostaining, Expressing, Western Blot

Journal: Bioactive Materials

Article Title: Tissue-specific matrix-bound nanovesicles regulate the immunoregulatory progress of biological mesh-aided abdominal hernia repair

doi: 10.1016/j.bioactmat.2026.03.004

Figure Lengend Snippet: Inflammatory immune responses following mesh implantation. A) Schematic illustration and representative macroscopic images of seroma tissues collected from the explants at 1 week. B) ELISA analysis of cytokines in the seroma fluid after 1 week (n = 4). C) Representative immunofluorescence images of CD11b + cell infiltration in mesh at 1 and 4 weeks. Scale bars: left, 1000 μm; right, 50 μm. D–E) Quantification of CD11b + cell density (n = 5, 4 samples per rat). F) Representative immunofluorescence images of CD68 (yellow), CD86 (green), and CD206 (red) staining of SIS and UBM-SIS at 1 and 4 weeks. Scale bars: top, 1000 μm; bottom, 50 μm. G–H) Quantification of CD68 + macrophage infiltration and M2-like/M1-like phenotypic distribution at 1 week (n = 5). I) Statistical comparison of M2-like/M1-like ratios between SIS and UBM-SIS groups (n = 5). J–K) CD68 + macrophage infiltration and CD206 + /CD86 + phenotypic distribution at 4 weeks (n = 5, 4 samples per rat). L) Quantification of M2-like/M1-like ratios at 4 weeks (n = 5, 4 samples per rat). M−O) Representative immunofluorescence images of iNOS and Arg-1 at tissue-mesh interfaces at 1 and 4 weeks, with quantitative analysis of positive area (n = 5, with 4 samples per rat). Scale bars: 50 μm. P) RT-qPCR analysis of pro- (( TNF-α, IL-6 ) and anti-inflammatory ( IL-10, TGF-β1 ) cytokine gene expression in SIS and UBM-SIS explants. Q) Schematic summary of immune response transition induced by SIS versus UBM-SIS MBV-containing meshes over 4 weeks. The asterisk indicates the implanted mesh. Data are presented as mean ± SD. For (B, I, L, and P), mean value of each rat (n = 5) was used for statistical comparisons. For (D, E, G, H, J, K, N, and O), each dot represents one section-level sample, where the value of each animal for statistical comparisons was obtained by averaging measurements from 4 samples. Statistical comparisons were performed within each time point using two-tailed unpaired Student's t-test, where ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001.

Techniques: Enzyme-linked Immunosorbent Assay, Immunofluorescence, Staining, Comparison, Quantitative RT-PCR, Gene Expression, Two Tailed Test

Journal: Bioactive Materials

Article Title: Tissue-specific matrix-bound nanovesicles regulate the immunoregulatory progress of biological mesh-aided abdominal hernia repair

doi: 10.1016/j.bioactmat.2026.03.004

Figure Lengend Snippet: ECM remodeling and mechanical evaluation of meshes and explants. A) Representative immunofluorescence images showing collagen I (red) and collagen III (green) deposition in the center and interface regions of SIS and UBM–SIS explants at 8 weeks. Scale bars: overview = 1000 μm, magnified images = 100 μm. B–E) Quantification of total collagen (I + III), collagen I, and collagen III positive expression and collagen I/III ratio in the center and interface regions (n = 5, 4 samples per rat). F–G) Polar plot of collagen fiber orientation in the center and interface regions analyzed by orientation distribution. H) Orientation coherency of collagen fibers in the center and interface regions (n = 5, 4 samples per rat). I) Aspect ratio analysis indicating collagen fibril anisotropy (n = 4). J–K) Representative immunofluorescence staining of TGF-β1 and α-SMA at 8 weeks and corresponding quantification of positive area (n = 5, 4 samples per rat). L, M) Mechanical characterization of meshes and explants showing ultimate tensile strength and elongation at break across different time points (n = 4). N) Comparison of tensile strength and elongation of explants with native abdominal wall components, including posterior and anterior rectus sheath, linea alba, peritoneum, and transversalis fascia. The asterisk indicates the implanted mesh. Data are presented as mean ± SD. For (B-E, H, and K), mean value of each rat (n = 5) was used for statistical comparisons. Each dot represents one section-level sample, where the value for each animal was obtained by averaging measurements from 4 samples. For (I, L, and M), mean value of each rat (n = 4) was used for statistical comparisons. Statistical significance was determined using two-tailed unpaired Student's t-test, where ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001.

Techniques: Immunofluorescence, Expressing, Staining, Comparison, Two Tailed Test

Journal: Bioactive Materials

Article Title: Tissue-specific matrix-bound nanovesicles regulate the immunoregulatory progress of biological mesh-aided abdominal hernia repair

doi: 10.1016/j.bioactmat.2026.03.004

Figure Lengend Snippet: Transcriptomic analysis of explants from different groups after 1 week and comparative analysis of MBV and ECM properties. A) Schematic illustration of tissues collected from the explants at 1 week for distinct signaling pathway analysis. B) Volcano plot showing differentially expressed genes (DEGs) between UBM-SIS and SIS groups (n = 3 per group). C) Heatmap of DEGs between SIS and UBM-SIS groups (red: upregulated, blue: downregulated; cutoff >1.0; n = 3). D) KEGG pathway enrichment analysis of downregulated genes in UBM-SIS compared to SIS. E) Reactome pathway enrichment analysis of downregulated genes in UBM-SIS compared to SIS. F–H) GSEA demonstrating altered gene signatures related to NET formation, NF-κB pathway and cytokine-cytokine receptor interaction. I) Radar plot comparing SIS- and UBM-derived MBVs. The five axes represent key pathways involved in angiogenesis ( ERK ), vascularization ( AKT ), inflammation ( p65 ), immunomodulation ( STAT3 ), and remodeling ( TGF-β/Smad ). J) Radar plot summarizing ECM in vivo performance at 1 and 4 weeks. The five axes represent essential features in ECM remodeling, including adhesion, angiogenesis, inflammation, immunomodulation, and collagen deposition.

Techniques: Derivative Assay, In Vivo

Ranitidine inhibits TGF-β1-induced total collagen accumulation in NIH/3T3 fibroblasts. Total collagen content was measured by Sirius red assay. Data are presented as mean ± SD from three independent experiments. *p < 0.05.

Journal: Frontiers in Pharmacology

Article Title: Ranitidine attenuates myocardial fibrosis by suppressing histamine/H2 receptor signaling and FAK/Src activation

doi: 10.3389/fphar.2026.1874499

Figure Lengend Snippet: Ranitidine inhibits TGF-β1-induced total collagen accumulation in NIH/3T3 fibroblasts. Total collagen content was measured by Sirius red assay. Data are presented as mean ± SD from three independent experiments. *p < 0.05.

Article Snippet: Key reagents included ranitidine (Macklin, R838252, purity >98%), valsartan (Macklin, V844023, purity >95%), and TGF-β1 (MedChemExpress, HY-P7117, purity >95%).

Techniques:

Ranitidine inhibits the expression of fibrosis-related proteins and reduces FAK/Src activation in TGF-β1-stimulated fibroblasts. (A) Representative Western blot images of p-FAK, FAK, p-Src, Src, α-SMA, Collagen I, Collagen III, and GAPDH in fibroblasts treated with TGF-β1 (15 ng/mL) with or without ranitidine (RN, 0.1, 1, and 10 μM). (B–D) Quantification of α-SMA, Collagen I, and Collagen III protein expression. (E,F) Quantification of p-FAK and p-Src protein expression. Data are presented as mean ± SD from three independent experiments. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001.

Journal: Frontiers in Pharmacology

Article Title: Ranitidine attenuates myocardial fibrosis by suppressing histamine/H2 receptor signaling and FAK/Src activation

doi: 10.3389/fphar.2026.1874499

Figure Lengend Snippet: Ranitidine inhibits the expression of fibrosis-related proteins and reduces FAK/Src activation in TGF-β1-stimulated fibroblasts. (A) Representative Western blot images of p-FAK, FAK, p-Src, Src, α-SMA, Collagen I, Collagen III, and GAPDH in fibroblasts treated with TGF-β1 (15 ng/mL) with or without ranitidine (RN, 0.1, 1, and 10 μM). (B–D) Quantification of α-SMA, Collagen I, and Collagen III protein expression. (E,F) Quantification of p-FAK and p-Src protein expression. Data are presented as mean ± SD from three independent experiments. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001.

Article Snippet: Key reagents included ranitidine (Macklin, R838252, purity >98%), valsartan (Macklin, V844023, purity >95%), and TGF-β1 (MedChemExpress, HY-P7117, purity >95%).

Techniques: Expressing, Activation Assay, Western Blot

Ranitidine reduces the mRNA expression of fibrosis-related markers in TGF-β1-stimulated fibroblasts. (A–C) Relative mRNA expression levels of α-SMA, Collagen I, and Collagen III in fibroblasts treated with TGF-β1 (15 ng/mL) with or without ranitidine (RN, 0.1, 1, and 10 μM). Data are presented as mean ± SD from three independent experiments. ***p < 0.001.

Journal: Frontiers in Pharmacology

Article Title: Ranitidine attenuates myocardial fibrosis by suppressing histamine/H2 receptor signaling and FAK/Src activation

doi: 10.3389/fphar.2026.1874499

Figure Lengend Snippet: Ranitidine reduces the mRNA expression of fibrosis-related markers in TGF-β1-stimulated fibroblasts. (A–C) Relative mRNA expression levels of α-SMA, Collagen I, and Collagen III in fibroblasts treated with TGF-β1 (15 ng/mL) with or without ranitidine (RN, 0.1, 1, and 10 μM). Data are presented as mean ± SD from three independent experiments. ***p < 0.001.

Article Snippet: Key reagents included ranitidine (Macklin, R838252, purity >98%), valsartan (Macklin, V844023, purity >95%), and TGF-β1 (MedChemExpress, HY-P7117, purity >95%).

Techniques: Expressing

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tgf β1 (Santa Cruz Biotechnology)

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