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primary antibodies against collagen i  (Proteintech)


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    Structured Review

    Proteintech primary antibodies against collagen i
    Primary Antibodies Against Collagen I, supplied by Proteintech, used in various techniques. Bioz Stars score: 96/100, based on 974 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/primary+antibodies+against+collagen+i/Collagen+Type+I+Polyclonal+antibody/pm41871675-115-0-5
    Average 96 stars, based on 974 article reviews
    primary antibodies against collagen i - by Bioz Stars, 2026-09
    96/100 stars

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    Related Articles

    Incubation:

    Article Title: Ectopic endometrial stromal cell-derived extracellular vesicles encapsulating microRNA-25-3p induce endometrial collagen I deposition impairing decidualization in endometriosis.
    Article Snippet: Endometrial collagen I undergoes dynamic degradation and remodelling in response to endometrial stromal cell (ESC) decidualization and embryo implantation.. However, excessive collagen I deposition in the endometrium during the implantation window may impair decidualization, causing embryo implantation failure in patients with endometriosis (EMS).. We found that endometrial collagen I expression during the mid-secretory phase was increased in the EMS group of patients.

    Article Title: Ulinastatin attenuates renal fibrosis by regulating AMPK/HIF-1α signaling pathway-mediated glycolysis.
    Article Snippet: .. After that, the proteins on the membranes were incubated overnight at 4 °C with the specific primary antibodies against Collagen I (no.67288-1-IG, 1:5000, Proteintech), α-smooth muscle actin (α-SMA, no.14395-1-AP, 1:5000, Proteintech), p-AMPKα (phospho Thr172, no. #50081S, 1:1000, CST), AMPKα (no.#2532S, 1:1000, CST), HIF-1α (no.BF8002, 1:500, Affinity), M2-pyruvate kinase (PKM2, no.15822-1-AP, 1:5000, Proteintech), Lactate dehydrogenase A (LDHA, no.19987-1-AP, 1:5000, Proteintech), and Tubulin (no.66031-1-lg, 1:60000, Proteintech). .. Next, horseradish peroxidase-conjugated goat anti-mouse (no.31430, 1:5000, Thermo Fisher Scientific) or anti-rabbit (no.31460, 1:5000, Thermo Fisher Scientific) secondary antibodies were added for 1 h. Finally, the specific immune blots were visualized using enhanced chemiluminescence (ProteinTech) and detected by the chemiluminescence imaging system (Tanon, China).

    Article Title: Microneedle-delivered ROS-adaptive asiatic acid nanoparticles promote scarless repair via remodeling the pathological microenvironment.
    Article Snippet: .. 340 SEI(%)= H scarH normal Equation (5) 341 For the immunohistochemical experiment, tissue sections were incubated with 342 primary antibodies against collagen I (Proteintech, 1:1000), collagen III (Proteintech, 343 1:1000), α-smooth muscle actin (α-SMA) (Haoke Biotechnology, 1:2500), Cytokeratin 344 6 (CK6) (Biolynx Biotechnology, 1:2500) at 4 °C overnight. .. Subsequently, the sections 345 were incubated with an HRP-conjugated secondary antibody (Haoke Biotechnology) for 346 one hour at 25 °C.

    Article Title: Ex Vivo Biosensor Strategy Reveals the Vascular Toxic Effects of Volatile Organic Compounds Derived from Indoor Renovation
    Article Snippet: After denaturation, proteins were separated by sodium dodecyl sulfate ‒ polyacrylamide gel electrophoresis (SDS‒PAGE) and transferred to polyvinylidene fluoride membranes (Merck & Co., Inc, New Jersey, USA). .. After being blocked for 4 h at room temperature, the blots were incubated with specific primary antibodies against collagen I (14695-1-AP, Proteintech, 1:1000), collagen III(A0817, ABclonal, 1:1000), OPN (YT3467, Immunoway, 1:1000), DNMT1 (A22455, ABclonal, 1:1000), cGAS (ARG40192, Arigo, 1:1000), STING (A3575, ABclonal, 1:1000), VDAC1 (ET-1601-20, HuaBio, 1:2000), α-SMA (A307717-01, Earthox, 1:1000), TNF-α (A300370-01, Earthox, 1:1500), IL-1 β (A1112, ABclone, 1:1000), IL-6 (21865-1-AP, proteintech, 1:1000) and GAPDH (10494-1-AP, Proteintech, 1:20000) at 4°C overnight. .. After washing four times with TBST, the membranes were incubated with secondary antibodies (S1001-100, SeraCare/KPL, 1:2000 and SA00001-2, Proteintech, 1:5000) were incubated at 37°C in an incubator for 1 h and then washed four times.

    Article Title: Ulinastatin attenuates renal fibrosis by regulating AMPK/HIF-1α signaling pathway-mediated glycolysis
    Article Snippet: .. After that, the proteins on the membranes were incubated overnight at 4 °C with the specific primary antibodies against Collagen I (no.67288-1-IG, 1:5000, Proteintech), α-smooth muscle actin (α-SMA, no.14395-1-AP, 1:5000, Proteintech), p-AMPKα (phospho Thr172, no. #50081S, 1:1000, CST), AMPKα (no.#2532S, 1:1000, CST), HIF-1α (no.BF8002, 1:500, Affinity), M2-pyruvate kinase (PKM2, no.15822-1-AP, 1:5000, Proteintech), Lactate dehydrogenase A (LDHA, no.19987-1-AP, 1:5000, Proteintech), and Tubulin (no.66031-1-lg, 1:60000, Proteintech). .. Next, horseradish peroxidase-conjugated goat anti-mouse (no.31430, 1:5000, Thermo Fisher Scientific) or anti-rabbit (no.31460, 1:5000, Thermo Fisher Scientific) secondary antibodies were added for 1 h. Finally, the specific immune blots were visualized using enhanced chemiluminescence (ProteinTech) and detected by the chemiluminescence imaging system (Tanon, China).

    Article Title: Mechanism of Curcumin in the Treatment of Intrauterine Adhesions Based on Network Pharmacology, Molecular docking, and Experimental Validation.
    Article Snippet: Intrauterine adhesions (IUA) is one of the most prevalent gynecological conditions affecting women of childbearing age.. The active ingredient curcumin (CUR), derived from turmeric, is a promising candidate for the treatment of IUA.. Nevertheless, the mechanism of action remains undetermined.

    Immunohistochemical staining:

    Article Title: Microneedle-delivered ROS-adaptive asiatic acid nanoparticles promote scarless repair via remodeling the pathological microenvironment.
    Article Snippet: .. 340 SEI(%)= H scarH normal Equation (5) 341 For the immunohistochemical experiment, tissue sections were incubated with 342 primary antibodies against collagen I (Proteintech, 1:1000), collagen III (Proteintech, 343 1:1000), α-smooth muscle actin (α-SMA) (Haoke Biotechnology, 1:2500), Cytokeratin 344 6 (CK6) (Biolynx Biotechnology, 1:2500) at 4 °C overnight. .. Subsequently, the sections 345 were incubated with an HRP-conjugated secondary antibody (Haoke Biotechnology) for 346 one hour at 25 °C.

    Blocking Assay:

    Article Title: Mechanism of Curcumin in the Treatment of Intrauterine Adhesions Based on Network Pharmacology, Molecular docking, and Experimental Validation.
    Article Snippet: Intrauterine adhesions (IUA) is one of the most prevalent gynecological conditions affecting women of childbearing age.. The active ingredient curcumin (CUR), derived from turmeric, is a promising candidate for the treatment of IUA.. Nevertheless, the mechanism of action remains undetermined.



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    Proteintech primary antibodies against collagen i
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    Proteintech primary antibodies against collagen 1
    The 3,5-diethoxycarbonyl-1,4-dihydrocollidine diet mouse model (4 weeks) exhibited moderate biliary fibrosis in the portal vein region. A: Hematoxylin-eosin, Masson, and Sirius red staining of mouse livers; B-G: Statistical analysis of Masson and Sirius red staining results; H: Immunohistochemistry staining for <t>collagen-1,</t> α-smooth muscle actin (SMA), and desmin in mouse livers; I-Q: Statistical analysis of collagen-1, α-SMA, and desmin staining results. Sample sizes ( n ): 8:8 (normal chow diet vs 3,5-diethoxycarbonyl-1,4-dihydrocollidine), 8:7 (sham vs bile duct ligation), and 8:7:8 (oil vs 8-week carbon tetrachloride vs 12-week carbon tetrachloride). a P < 0.05. b P < 0.01. c P < 0.001. NS: No significant; NCD: Normal chow diet; DDC: 3,5-diethoxycarbonyl-1,4-dihydrocollidine; BDL: Bile duct ligation; CCl 4 : Carbon tetrachloride; HE: Hematoxylin-eosin; COL1: Collagen-1; SMA: Smooth muscle actin.
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    Servicebio Inc mouse primary antibodies against collagen i
    The 3,5-diethoxycarbonyl-1,4-dihydrocollidine diet mouse model (4 weeks) exhibited moderate biliary fibrosis in the portal vein region. A: Hematoxylin-eosin, Masson, and Sirius red staining of mouse livers; B-G: Statistical analysis of Masson and Sirius red staining results; H: Immunohistochemistry staining for <t>collagen-1,</t> α-smooth muscle actin (SMA), and desmin in mouse livers; I-Q: Statistical analysis of collagen-1, α-SMA, and desmin staining results. Sample sizes ( n ): 8:8 (normal chow diet vs 3,5-diethoxycarbonyl-1,4-dihydrocollidine), 8:7 (sham vs bile duct ligation), and 8:7:8 (oil vs 8-week carbon tetrachloride vs 12-week carbon tetrachloride). a P < 0.05. b P < 0.01. c P < 0.001. NS: No significant; NCD: Normal chow diet; DDC: 3,5-diethoxycarbonyl-1,4-dihydrocollidine; BDL: Bile duct ligation; CCl 4 : Carbon tetrachloride; HE: Hematoxylin-eosin; COL1: Collagen-1; SMA: Smooth muscle actin.
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    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 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Proteintech primary antibodies against col i
    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 Antibodies Against Col I, supplied by Proteintech, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Huabio Inc primary antibodies against collagen i
    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 Antibodies Against Collagen I, supplied by Huabio Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Proteintech primary antibodies against col 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 Antibodies Against Col 1, supplied by Proteintech, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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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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    Proteintech primary antibodies against coli
    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


    The 3,5-diethoxycarbonyl-1,4-dihydrocollidine diet mouse model (4 weeks) exhibited moderate biliary fibrosis in the portal vein region. A: Hematoxylin-eosin, Masson, and Sirius red staining of mouse livers; B-G: Statistical analysis of Masson and Sirius red staining results; H: Immunohistochemistry staining for collagen-1, α-smooth muscle actin (SMA), and desmin in mouse livers; I-Q: Statistical analysis of collagen-1, α-SMA, and desmin staining results. Sample sizes ( n ): 8:8 (normal chow diet vs 3,5-diethoxycarbonyl-1,4-dihydrocollidine), 8:7 (sham vs bile duct ligation), and 8:7:8 (oil vs 8-week carbon tetrachloride vs 12-week carbon tetrachloride). a P < 0.05. b P < 0.01. c P < 0.001. NS: No significant; NCD: Normal chow diet; DDC: 3,5-diethoxycarbonyl-1,4-dihydrocollidine; BDL: Bile duct ligation; CCl 4 : Carbon tetrachloride; HE: Hematoxylin-eosin; COL1: Collagen-1; SMA: Smooth muscle actin.

    Journal: World Journal of Gastroenterology

    Article Title: Evaluation of a 3,5-diethoxycarbonyl-1,4-dihydrocollidine diet-induced mouse model in a comparative experimental study of portal hypertension

    doi: 10.3748/wjg.v32.i9.114207

    Figure Lengend Snippet: The 3,5-diethoxycarbonyl-1,4-dihydrocollidine diet mouse model (4 weeks) exhibited moderate biliary fibrosis in the portal vein region. A: Hematoxylin-eosin, Masson, and Sirius red staining of mouse livers; B-G: Statistical analysis of Masson and Sirius red staining results; H: Immunohistochemistry staining for collagen-1, α-smooth muscle actin (SMA), and desmin in mouse livers; I-Q: Statistical analysis of collagen-1, α-SMA, and desmin staining results. Sample sizes ( n ): 8:8 (normal chow diet vs 3,5-diethoxycarbonyl-1,4-dihydrocollidine), 8:7 (sham vs bile duct ligation), and 8:7:8 (oil vs 8-week carbon tetrachloride vs 12-week carbon tetrachloride). a P < 0.05. b P < 0.01. c P < 0.001. NS: No significant; NCD: Normal chow diet; DDC: 3,5-diethoxycarbonyl-1,4-dihydrocollidine; BDL: Bile duct ligation; CCl 4 : Carbon tetrachloride; HE: Hematoxylin-eosin; COL1: Collagen-1; SMA: Smooth muscle actin.

    Article Snippet: Primary antibodies against collagen 1 (1:2500, catalog No. 67288-1-Ig, Proteintech), α-smooth muscle actin (SMA) (1:200, catalog No. ab5694, Abcam), desmin (1:4000, catalog No. 16520-1-AP, Proteintech), lymphatic vessel endothelial hyaluronan receptor 1 (LyVE-1) (1:100, catalog No. ab219556, Abcam), cluster of differentiation (CD) 34 (1:1000, catalog No. 14486-1-AP, Proteintech), von Willebrand factor (vWF) (1:200, catalog No. 27186-1-AP, Proteintech), vascular endothelial growth factor receptor 2 (VEGFR2) (1:150, catalog No. ab2349, Abcam), vascular endothelial growth factor A (VEGF-A) (1:100, catalog No. ab52917, Abcam), and CD31 (1:5000, catalog No. 11265-1-AP, Proteintech) were applied overnight at 4 °C, followed by 60-minute incubation with secondary antibodies at room temperature.

    Techniques: Staining, Immunohistochemistry, Ligation

    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