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tgf β  (Elabscience Biotechnology)


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    Structured Review

    Elabscience Biotechnology tgf β
    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 <t>(TGF-β,</t> <t>PGE2,</t> 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.
    Tgf β, supplied by Elabscience Biotechnology, used in various techniques. Bioz Stars score: 96/100, based on 331 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/tgf β/product/Elabscience Biotechnology
    Average 96 stars, based on 331 article reviews
    tgf β - by Bioz Stars, 2026-05
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    Images

    1) Product Images from "Mesenchymal stromal cells-loaded 3D radially aligned composite scaffold with potentiated paracrine signaling for sequential bone regeneration"

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

    Journal: Bioactive Materials

    doi: 10.1016/j.bioactmat.2026.02.059

    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.
    Figure Legend 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.

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



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    Exercise <t>modulates</t> <t>TGF-β1</t> expression in the prefrontal cortex (PFC) of mice 24 days after spared nerve injury (SNI). (a) Representative Western blot images of TGF-β receptor I (TGF-βR1) and TGF-β1 in the PFC. Tissue lysates from all experimental groups (SHAM, SHAME, SNI, SNIE) and recombinant human TGF-β1 (non-reduced and reduced) were loaded on the same SDS–PAGE gel, transferred to a single membrane, and probed with the same TGF-β1 antibody under identical exposure conditions. The recombinant protein (250 ng per lane) served as a positive control to verify the molecular weights of the dimeric (25 kDa) and monomeric (12.5 kDa) forms of TGF-β1. GAPDH was used as the loading control. (b-d) Quantitative Western blot analyses of (b) TGF-βR1, (c) dimeric TGF-β1 (25 kDa), and (d) monomeric TGF-β1 (12.5 kDa) expression levels in tissue lysates. Data are presented as mean ± SEM (n = 3). ** P < 0.01 vs. SHAM group; ## P < 0.01 vs. SNI group.
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    Exercise <t>modulates</t> <t>TGF-β1</t> expression in the prefrontal cortex (PFC) of mice 24 days after spared nerve injury (SNI). (a) Representative Western blot images of TGF-β receptor I (TGF-βR1) and TGF-β1 in the PFC. Tissue lysates from all experimental groups (SHAM, SHAME, SNI, SNIE) and recombinant human TGF-β1 (non-reduced and reduced) were loaded on the same SDS–PAGE gel, transferred to a single membrane, and probed with the same TGF-β1 antibody under identical exposure conditions. The recombinant protein (250 ng per lane) served as a positive control to verify the molecular weights of the dimeric (25 kDa) and monomeric (12.5 kDa) forms of TGF-β1. GAPDH was used as the loading control. (b-d) Quantitative Western blot analyses of (b) TGF-βR1, (c) dimeric TGF-β1 (25 kDa), and (d) monomeric TGF-β1 (12.5 kDa) expression levels in tissue lysates. Data are presented as mean ± SEM (n = 3). ** P < 0.01 vs. SHAM group; ## P < 0.01 vs. SNI group.
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    Image Search Results


    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.

    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

    Exercise modulates TGF-β1 expression in the prefrontal cortex (PFC) of mice 24 days after spared nerve injury (SNI). (a) Representative Western blot images of TGF-β receptor I (TGF-βR1) and TGF-β1 in the PFC. Tissue lysates from all experimental groups (SHAM, SHAME, SNI, SNIE) and recombinant human TGF-β1 (non-reduced and reduced) were loaded on the same SDS–PAGE gel, transferred to a single membrane, and probed with the same TGF-β1 antibody under identical exposure conditions. The recombinant protein (250 ng per lane) served as a positive control to verify the molecular weights of the dimeric (25 kDa) and monomeric (12.5 kDa) forms of TGF-β1. GAPDH was used as the loading control. (b-d) Quantitative Western blot analyses of (b) TGF-βR1, (c) dimeric TGF-β1 (25 kDa), and (d) monomeric TGF-β1 (12.5 kDa) expression levels in tissue lysates. Data are presented as mean ± SEM (n = 3). ** P < 0.01 vs. SHAM group; ## P < 0.01 vs. SNI group.

    Journal: IBRO Neuroscience Reports

    Article Title: TGF-β1 modulates PFC glial cell activation to facilitate exercise-induced analgesia in mice with spared nerve injury

    doi: 10.1016/j.ibneur.2026.03.009

    Figure Lengend Snippet: Exercise modulates TGF-β1 expression in the prefrontal cortex (PFC) of mice 24 days after spared nerve injury (SNI). (a) Representative Western blot images of TGF-β receptor I (TGF-βR1) and TGF-β1 in the PFC. Tissue lysates from all experimental groups (SHAM, SHAME, SNI, SNIE) and recombinant human TGF-β1 (non-reduced and reduced) were loaded on the same SDS–PAGE gel, transferred to a single membrane, and probed with the same TGF-β1 antibody under identical exposure conditions. The recombinant protein (250 ng per lane) served as a positive control to verify the molecular weights of the dimeric (25 kDa) and monomeric (12.5 kDa) forms of TGF-β1. GAPDH was used as the loading control. (b-d) Quantitative Western blot analyses of (b) TGF-βR1, (c) dimeric TGF-β1 (25 kDa), and (d) monomeric TGF-β1 (12.5 kDa) expression levels in tissue lysates. Data are presented as mean ± SEM (n = 3). ** P < 0.01 vs. SHAM group; ## P < 0.01 vs. SNI group.

    Article Snippet: To validate the specificity of the TGF-β1 antibody, Recombinant human TGF-β1 protein (Catalog # 240-B, R&D Systems, USA) was used as a positive control.

    Techniques: Expressing, Western Blot, Recombinant, SDS Page, Membrane, Positive Control, Control

    At 24 d after SNI, mouse PFC astrocytes were activated and microglia were unchanged. (a)Western blotting analysis of changes in GFAP and Iba1 expression in PFC (n = 3); (b) Quantification of GFAP in PFC; (c) Quantification of Iba1 in PFC; (d) MFI representative images of GFAP in PFC; (e) MFI representative image of Iba1 in PFC; (f) Quantification of GFAP in PFC. Values represent mean ± SEM (Scale bar =75μm, 9 PFC sections from 3 mice per group); (g) Quantification of Iba1 in PFC. Values represent mean ±SEM (Scale bar = 75μm, 9 PFC sections from 3 mice per group). Values represent the mean ±SEM. * P < 0.05, ** P < 0.01, compared with SHAM group; # P < 0.05, ## P < 0.01, compared with SNI group, the difference was statistically significant; (h) Representative MFI images of changes in the colocalization of TGF-β1(red) and astrocytes (green) in the PFC; (i) Quantification of TGF-β1 and astrocytes in PFC. Values represent the mean ± SEM (Scale bar =100μm, nine PFC sections from three mice per group). * P < 0.05 versus the SHAM group; # P < 0.05 versus the SNI group.

    Journal: IBRO Neuroscience Reports

    Article Title: TGF-β1 modulates PFC glial cell activation to facilitate exercise-induced analgesia in mice with spared nerve injury

    doi: 10.1016/j.ibneur.2026.03.009

    Figure Lengend Snippet: At 24 d after SNI, mouse PFC astrocytes were activated and microglia were unchanged. (a)Western blotting analysis of changes in GFAP and Iba1 expression in PFC (n = 3); (b) Quantification of GFAP in PFC; (c) Quantification of Iba1 in PFC; (d) MFI representative images of GFAP in PFC; (e) MFI representative image of Iba1 in PFC; (f) Quantification of GFAP in PFC. Values represent mean ± SEM (Scale bar =75μm, 9 PFC sections from 3 mice per group); (g) Quantification of Iba1 in PFC. Values represent mean ±SEM (Scale bar = 75μm, 9 PFC sections from 3 mice per group). Values represent the mean ±SEM. * P < 0.05, ** P < 0.01, compared with SHAM group; # P < 0.05, ## P < 0.01, compared with SNI group, the difference was statistically significant; (h) Representative MFI images of changes in the colocalization of TGF-β1(red) and astrocytes (green) in the PFC; (i) Quantification of TGF-β1 and astrocytes in PFC. Values represent the mean ± SEM (Scale bar =100μm, nine PFC sections from three mice per group). * P < 0.05 versus the SHAM group; # P < 0.05 versus the SNI group.

    Article Snippet: To validate the specificity of the TGF-β1 antibody, Recombinant human TGF-β1 protein (Catalog # 240-B, R&D Systems, USA) was used as a positive control.

    Techniques: Western Blot, Expressing

    TGF-βRI inhibition reverses exercise-induced analgesia and modulates glial activation in the PFC. (a, b) Time course of mechanical and cold hyperalgesia tests (n = 9). The green shading indicates the duration of the exercise intervention, and the green vertical lines denote the timing of intrathecal injections. Data are presented as mean ± SEM. ** P < 0.01 versus the SNIE group, # P < 0.05, ## P < 0.01 vs. SC group. (c) Representative Western blot images of TGF-βR1 and TGF-β1 in the PFC. Tissue lysates from SC and SA groups and recombinant human TGF-β1 (100 ng per lane) (non-reduced and reduced) were loaded on the same SDS–PAGE gel, transferred to a single membrane, and probed with the same TGF-β1 antibody in a single exposure without splicing. The recombinant protein served as a positive control to verify the molecular weights of the dimeric (25 kDa) and monomeric (12.5 kDa) forms of TGF-β1. GAPDH was used as the loading control. (d-f) Quantitative analysis of (d) TGF-βR1, (e) dimeric TGF-β1 (25 kDa), and (f) monomeric TGF-β1 (12.5 kDa) expression levels (n = 3). (g-i) Western blot analysis of glial markers. (g) Representative images of GFAP and Iba1 with GAPDH control. Quantitative analysis of (h) GFAP and (i) Iba1 expression levels (n = 3). (j, k) Representative immunofluorescence images showing the expression of (j) GFAP and (k) Iba1 in the PFC. Scale bar = 75 μm. (l, m) Quantification of the mean fluorescence intensity (MFI) for (l) GFAP and (m) Iba1 (n = 9 sections from 3 mice per group). Data in bar graphs are presented as mean ± SEM. * P < 0.05, ** P < 0.01 vs. SC group. SC: Spared nerve injury with exercise training followed by intrathecal (i.t.) injection of saline; SA: Spared nerve injury with exercise training followed by i.t. injection of the TGF-βRI inhibitor.

    Journal: IBRO Neuroscience Reports

    Article Title: TGF-β1 modulates PFC glial cell activation to facilitate exercise-induced analgesia in mice with spared nerve injury

    doi: 10.1016/j.ibneur.2026.03.009

    Figure Lengend Snippet: TGF-βRI inhibition reverses exercise-induced analgesia and modulates glial activation in the PFC. (a, b) Time course of mechanical and cold hyperalgesia tests (n = 9). The green shading indicates the duration of the exercise intervention, and the green vertical lines denote the timing of intrathecal injections. Data are presented as mean ± SEM. ** P < 0.01 versus the SNIE group, # P < 0.05, ## P < 0.01 vs. SC group. (c) Representative Western blot images of TGF-βR1 and TGF-β1 in the PFC. Tissue lysates from SC and SA groups and recombinant human TGF-β1 (100 ng per lane) (non-reduced and reduced) were loaded on the same SDS–PAGE gel, transferred to a single membrane, and probed with the same TGF-β1 antibody in a single exposure without splicing. The recombinant protein served as a positive control to verify the molecular weights of the dimeric (25 kDa) and monomeric (12.5 kDa) forms of TGF-β1. GAPDH was used as the loading control. (d-f) Quantitative analysis of (d) TGF-βR1, (e) dimeric TGF-β1 (25 kDa), and (f) monomeric TGF-β1 (12.5 kDa) expression levels (n = 3). (g-i) Western blot analysis of glial markers. (g) Representative images of GFAP and Iba1 with GAPDH control. Quantitative analysis of (h) GFAP and (i) Iba1 expression levels (n = 3). (j, k) Representative immunofluorescence images showing the expression of (j) GFAP and (k) Iba1 in the PFC. Scale bar = 75 μm. (l, m) Quantification of the mean fluorescence intensity (MFI) for (l) GFAP and (m) Iba1 (n = 9 sections from 3 mice per group). Data in bar graphs are presented as mean ± SEM. * P < 0.05, ** P < 0.01 vs. SC group. SC: Spared nerve injury with exercise training followed by intrathecal (i.t.) injection of saline; SA: Spared nerve injury with exercise training followed by i.t. injection of the TGF-βRI inhibitor.

    Article Snippet: To validate the specificity of the TGF-β1 antibody, Recombinant human TGF-β1 protein (Catalog # 240-B, R&D Systems, USA) was used as a positive control.

    Techniques: Inhibition, Activation Assay, Western Blot, Recombinant, SDS Page, Membrane, Positive Control, Control, Expressing, Immunofluorescence, Fluorescence, Injection, Saline