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primary polyclonal rabbit antibodies against collagen 1  (Proteintech)


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    Structured Review

    Proteintech primary polyclonal rabbit antibodies against collagen 1
    Inhibition of TNF- α mitigates glucose fluctuations-induced aortic valve fibrosis . (A,B,D,E) Immunohistochemical staining for <t>collagen</t> <t>1</t> and 3 (indicated by arrows) demonstrated enhanced collagen deposition in the aortic valves of the HG and GF diabetic rat models. However, treatment with infliximab was observed to mitigate this collagen accumulation. (C,F) Immunohistochemical analysis for α -SMA (arrows) revealed an increased fibrotic response in the aortic valves of the diabetic rats in the HG and GF groups; however, infliximab treatment reduced this progression (n = 5 per group). The data are presented as the mean ± SEM. Statistical analyses were conducted utilizing one-way ANOVA, followed by post hoc corrections to account for multiple comparisons (Fig. D–F). * p < 0.05, scale bar = 50 µm or 100 µm. α -SMA, α -smooth muscle actin.
    Primary Polyclonal Rabbit Antibodies Against Collagen 1, supplied by Proteintech, used in various techniques. Bioz Stars score: 96/100, based on 894 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/primary polyclonal rabbit antibodies against collagen 1/product/Proteintech
    Average 96 stars, based on 894 article reviews
    primary polyclonal rabbit antibodies against collagen 1 - by Bioz Stars, 2026-06
    96/100 stars

    Images

    1) Product Images from "Targeting Tumor Necrosis Factor-α Mitigates Glucose Fluctuation-Induced Aortic Valve Fibrosis: Insights From Diabetic Rat Models"

    Article Title: Targeting Tumor Necrosis Factor-α Mitigates Glucose Fluctuation-Induced Aortic Valve Fibrosis: Insights From Diabetic Rat Models

    Journal: Reviews in Cardiovascular Medicine

    doi: 10.31083/RCM42804

    Inhibition of TNF- α mitigates glucose fluctuations-induced aortic valve fibrosis . (A,B,D,E) Immunohistochemical staining for collagen 1 and 3 (indicated by arrows) demonstrated enhanced collagen deposition in the aortic valves of the HG and GF diabetic rat models. However, treatment with infliximab was observed to mitigate this collagen accumulation. (C,F) Immunohistochemical analysis for α -SMA (arrows) revealed an increased fibrotic response in the aortic valves of the diabetic rats in the HG and GF groups; however, infliximab treatment reduced this progression (n = 5 per group). The data are presented as the mean ± SEM. Statistical analyses were conducted utilizing one-way ANOVA, followed by post hoc corrections to account for multiple comparisons (Fig. D–F). * p < 0.05, scale bar = 50 µm or 100 µm. α -SMA, α -smooth muscle actin.
    Figure Legend Snippet: Inhibition of TNF- α mitigates glucose fluctuations-induced aortic valve fibrosis . (A,B,D,E) Immunohistochemical staining for collagen 1 and 3 (indicated by arrows) demonstrated enhanced collagen deposition in the aortic valves of the HG and GF diabetic rat models. However, treatment with infliximab was observed to mitigate this collagen accumulation. (C,F) Immunohistochemical analysis for α -SMA (arrows) revealed an increased fibrotic response in the aortic valves of the diabetic rats in the HG and GF groups; however, infliximab treatment reduced this progression (n = 5 per group). The data are presented as the mean ± SEM. Statistical analyses were conducted utilizing one-way ANOVA, followed by post hoc corrections to account for multiple comparisons (Fig. D–F). * p < 0.05, scale bar = 50 µm or 100 µm. α -SMA, α -smooth muscle actin.

    Techniques Used: Inhibition, Immunohistochemical staining, Staining

    TNF- α -mediated inflammation could exacerbate fibrosis in vitro in porcine aortic valve interstitial cells across different glucose levels . (A,B,E,F) In the primary porcine aortic valve interstitial cells (pAVICs) groups, both HG and GF conditions were found to upregulate collagen 1 protein expression. Moreover, the proinflammatory cytokine TNF- α aggravated this upregulation under HG conditions, with an even more pronounced effect observed under GF conditions. Conversely, the inhibition of TNF- α could reverse these upregulations in both the HG and GF groups. (C,D,G,H) TGF- β 1 protein expression increased under both HG and GF conditions, with TNF- α further enhancing this increase, especially under GF conditions. The inhibition of TNF- α reversed these effects in both groups (n = 4 per group). The data are presented as the mean ± SEM. Statistical analyses were conducted utilizing one-way ANOVA, followed by post hoc corrections to account for multiple comparisons (Fig. E–H). * p < 0.05.
    Figure Legend Snippet: TNF- α -mediated inflammation could exacerbate fibrosis in vitro in porcine aortic valve interstitial cells across different glucose levels . (A,B,E,F) In the primary porcine aortic valve interstitial cells (pAVICs) groups, both HG and GF conditions were found to upregulate collagen 1 protein expression. Moreover, the proinflammatory cytokine TNF- α aggravated this upregulation under HG conditions, with an even more pronounced effect observed under GF conditions. Conversely, the inhibition of TNF- α could reverse these upregulations in both the HG and GF groups. (C,D,G,H) TGF- β 1 protein expression increased under both HG and GF conditions, with TNF- α further enhancing this increase, especially under GF conditions. The inhibition of TNF- α reversed these effects in both groups (n = 4 per group). The data are presented as the mean ± SEM. Statistical analyses were conducted utilizing one-way ANOVA, followed by post hoc corrections to account for multiple comparisons (Fig. E–H). * p < 0.05.

    Techniques Used: In Vitro, Expressing, Inhibition



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    Inhibition of TNF- α mitigates glucose fluctuations-induced aortic valve fibrosis . (A,B,D,E) Immunohistochemical staining for <t>collagen</t> <t>1</t> and 3 (indicated by arrows) demonstrated enhanced collagen deposition in the aortic valves of the HG and GF diabetic rat models. However, treatment with infliximab was observed to mitigate this collagen accumulation. (C,F) Immunohistochemical analysis for α -SMA (arrows) revealed an increased fibrotic response in the aortic valves of the diabetic rats in the HG and GF groups; however, infliximab treatment reduced this progression (n = 5 per group). The data are presented as the mean ± SEM. Statistical analyses were conducted utilizing one-way ANOVA, followed by post hoc corrections to account for multiple comparisons (Fig. D–F). * p < 0.05, scale bar = 50 µm or 100 µm. α -SMA, α -smooth muscle actin.
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    Inhibition of TNF- α mitigates glucose fluctuations-induced aortic valve fibrosis . (A,B,D,E) Immunohistochemical staining for <t>collagen</t> <t>1</t> and 3 (indicated by arrows) demonstrated enhanced collagen deposition in the aortic valves of the HG and GF diabetic rat models. However, treatment with infliximab was observed to mitigate this collagen accumulation. (C,F) Immunohistochemical analysis for α -SMA (arrows) revealed an increased fibrotic response in the aortic valves of the diabetic rats in the HG and GF groups; however, infliximab treatment reduced this progression (n = 5 per group). The data are presented as the mean ± SEM. Statistical analyses were conducted utilizing one-way ANOVA, followed by post hoc corrections to account for multiple comparisons (Fig. D–F). * p < 0.05, scale bar = 50 µm or 100 µm. α -SMA, α -smooth muscle actin.
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    Inhibition of TNF- α mitigates glucose fluctuations-induced aortic valve fibrosis . (A,B,D,E) Immunohistochemical staining for <t>collagen</t> <t>1</t> and 3 (indicated by arrows) demonstrated enhanced collagen deposition in the aortic valves of the HG and GF diabetic rat models. However, treatment with infliximab was observed to mitigate this collagen accumulation. (C,F) Immunohistochemical analysis for α -SMA (arrows) revealed an increased fibrotic response in the aortic valves of the diabetic rats in the HG and GF groups; however, infliximab treatment reduced this progression (n = 5 per group). The data are presented as the mean ± SEM. Statistical analyses were conducted utilizing one-way ANOVA, followed by post hoc corrections to account for multiple comparisons (Fig. D–F). * p < 0.05, scale bar = 50 µm or 100 µm. α -SMA, α -smooth muscle actin.
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    Image Search Results


    Inhibition of TNF- α mitigates glucose fluctuations-induced aortic valve fibrosis . (A,B,D,E) Immunohistochemical staining for collagen 1 and 3 (indicated by arrows) demonstrated enhanced collagen deposition in the aortic valves of the HG and GF diabetic rat models. However, treatment with infliximab was observed to mitigate this collagen accumulation. (C,F) Immunohistochemical analysis for α -SMA (arrows) revealed an increased fibrotic response in the aortic valves of the diabetic rats in the HG and GF groups; however, infliximab treatment reduced this progression (n = 5 per group). The data are presented as the mean ± SEM. Statistical analyses were conducted utilizing one-way ANOVA, followed by post hoc corrections to account for multiple comparisons (Fig. D–F). * p < 0.05, scale bar = 50 µm or 100 µm. α -SMA, α -smooth muscle actin.

    Journal: Reviews in Cardiovascular Medicine

    Article Title: Targeting Tumor Necrosis Factor-α Mitigates Glucose Fluctuation-Induced Aortic Valve Fibrosis: Insights From Diabetic Rat Models

    doi: 10.31083/RCM42804

    Figure Lengend Snippet: Inhibition of TNF- α mitigates glucose fluctuations-induced aortic valve fibrosis . (A,B,D,E) Immunohistochemical staining for collagen 1 and 3 (indicated by arrows) demonstrated enhanced collagen deposition in the aortic valves of the HG and GF diabetic rat models. However, treatment with infliximab was observed to mitigate this collagen accumulation. (C,F) Immunohistochemical analysis for α -SMA (arrows) revealed an increased fibrotic response in the aortic valves of the diabetic rats in the HG and GF groups; however, infliximab treatment reduced this progression (n = 5 per group). The data are presented as the mean ± SEM. Statistical analyses were conducted utilizing one-way ANOVA, followed by post hoc corrections to account for multiple comparisons (Fig. D–F). * p < 0.05, scale bar = 50 µm or 100 µm. α -SMA, α -smooth muscle actin.

    Article Snippet: Additionally, primary polyclonal rabbit antibodies against collagen 1 (14695-1-AP, Proteintech Group, Inc., Chicago, IL, USA) and collagen 3 (227345-1-AP, Proteintech Group, Inc., Chicago, IL, USA) were procured from Proteintech, USA.

    Techniques: Inhibition, Immunohistochemical staining, Staining

    TNF- α -mediated inflammation could exacerbate fibrosis in vitro in porcine aortic valve interstitial cells across different glucose levels . (A,B,E,F) In the primary porcine aortic valve interstitial cells (pAVICs) groups, both HG and GF conditions were found to upregulate collagen 1 protein expression. Moreover, the proinflammatory cytokine TNF- α aggravated this upregulation under HG conditions, with an even more pronounced effect observed under GF conditions. Conversely, the inhibition of TNF- α could reverse these upregulations in both the HG and GF groups. (C,D,G,H) TGF- β 1 protein expression increased under both HG and GF conditions, with TNF- α further enhancing this increase, especially under GF conditions. The inhibition of TNF- α reversed these effects in both groups (n = 4 per group). The data are presented as the mean ± SEM. Statistical analyses were conducted utilizing one-way ANOVA, followed by post hoc corrections to account for multiple comparisons (Fig. E–H). * p < 0.05.

    Journal: Reviews in Cardiovascular Medicine

    Article Title: Targeting Tumor Necrosis Factor-α Mitigates Glucose Fluctuation-Induced Aortic Valve Fibrosis: Insights From Diabetic Rat Models

    doi: 10.31083/RCM42804

    Figure Lengend Snippet: TNF- α -mediated inflammation could exacerbate fibrosis in vitro in porcine aortic valve interstitial cells across different glucose levels . (A,B,E,F) In the primary porcine aortic valve interstitial cells (pAVICs) groups, both HG and GF conditions were found to upregulate collagen 1 protein expression. Moreover, the proinflammatory cytokine TNF- α aggravated this upregulation under HG conditions, with an even more pronounced effect observed under GF conditions. Conversely, the inhibition of TNF- α could reverse these upregulations in both the HG and GF groups. (C,D,G,H) TGF- β 1 protein expression increased under both HG and GF conditions, with TNF- α further enhancing this increase, especially under GF conditions. The inhibition of TNF- α reversed these effects in both groups (n = 4 per group). The data are presented as the mean ± SEM. Statistical analyses were conducted utilizing one-way ANOVA, followed by post hoc corrections to account for multiple comparisons (Fig. E–H). * p < 0.05.

    Article Snippet: Additionally, primary polyclonal rabbit antibodies against collagen 1 (14695-1-AP, Proteintech Group, Inc., Chicago, IL, USA) and collagen 3 (227345-1-AP, Proteintech Group, Inc., Chicago, IL, USA) were procured from Proteintech, USA.

    Techniques: In Vitro, Expressing, Inhibition