rabbit anti er alpha (Rockland Immunochemicals)

Rockland Immunochemicals rabbit anti er alpha
Rabbit Anti Er Alpha, supplied by Rockland Immunochemicals, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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tnf α (Boster Bio)

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Tnf α, supplied by Boster Bio, 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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nf α rat specific elisa kit (Boster Bio)

Boster Bio nf α rat specific elisa kit
Nf α Rat Specific Elisa Kit, supplied by Boster Bio, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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tnf α elisa kit (Shanghai Korain Biotech Co Ltd)

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Tnf α Elisa Kit, supplied by Shanghai Korain Biotech Co Ltd, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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serum tumor necrosis factor α tnf α (Shanghai Korain Biotech Co Ltd)

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Serum Tumor Necrosis Factor α Tnf α, supplied by Shanghai Korain Biotech Co Ltd, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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human tnf α enzyme linked immunosorbent assay elisa kit (Boster Bio)

Boster Bio human tnf α enzyme linked immunosorbent assay elisa kit

Inhibition of <t>TNF-</t> α attenuates glucose fluctuations-induced proteoglycan deposition in the aortic valves of diabetic rat models . (A) HE staining was utilized to examine the morphology of the tricuspid aortic valves across five cohorts of diabetic rats. (B,C) Modified Movat–Russell pentachrome staining demonstrated an increased deposition of proteoglycans (indicated by arrows) in the aortic valves of the HG and GF rat cohorts in comparison to the CTRL cohort. However, administration of infliximab reduced proteoglycans (arrows) in both the HG and GF groups (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. C). * p < 0.05, scale bar = 100 µm. <t>TNF-</t> <t>α</t> , <t>tumor</t> <t>necrosis</t> <t>factor</t> alpha; HE, hematoxylin and eosin; ANOVA, analysis of variance.

Human Tnf α Enzyme Linked Immunosorbent Assay Elisa Kit, supplied by Boster Bio, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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anti tnf α primary antibody (Boster Bio)

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Anti Tnf α Primary Antibody, supplied by Boster Bio, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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anti tnf α (ProSci Incorporated)

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anti tnf α monoclonal antibody (Boster Bio)

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anti tnf α antibody (Boster Bio)

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Anti Tnf α Antibody, supplied by Boster Bio, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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anti tnf (ProSci Incorporated)

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Image Search Results

Inhibition of TNF- α attenuates glucose fluctuations-induced proteoglycan deposition in the aortic valves of diabetic rat models . (A) HE staining was utilized to examine the morphology of the tricuspid aortic valves across five cohorts of diabetic rats. (B,C) Modified Movat–Russell pentachrome staining demonstrated an increased deposition of proteoglycans (indicated by arrows) in the aortic valves of the HG and GF rat cohorts in comparison to the CTRL cohort. However, administration of infliximab reduced proteoglycans (arrows) in both the HG and GF groups (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. C). * p < 0.05, scale bar = 100 µm. TNF- α , tumor necrosis factor alpha; HE, hematoxylin and eosin; ANOVA, analysis of variance.

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 attenuates glucose fluctuations-induced proteoglycan deposition in the aortic valves of diabetic rat models . (A) HE staining was utilized to examine the morphology of the tricuspid aortic valves across five cohorts of diabetic rats. (B,C) Modified Movat–Russell pentachrome staining demonstrated an increased deposition of proteoglycans (indicated by arrows) in the aortic valves of the HG and GF rat cohorts in comparison to the CTRL cohort. However, administration of infliximab reduced proteoglycans (arrows) in both the HG and GF groups (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. C). * p < 0.05, scale bar = 100 µm. TNF- α , tumor necrosis factor alpha; HE, hematoxylin and eosin; ANOVA, analysis of variance.

Article Snippet: In addition, the concentrated SABC-POD (Mouse/Rabbit IgG) kit (SA2010, BOSTER Biological Technology Co., Ltd., Wuhan, China), DyLight 488 conjugated AffiniPure goat anti-mouse IgG (H + L) (BA1126, BOSTER Biological Technology Co., Ltd., Wuhan, China), DyLight 594 conjugated AffiniPure goat anti-rabbit IgG (H + L) (BA1142, BOSTER Biological Technology Co., Ltd., Wuhan, China), ethylenediaminetetraacetic acid (EDTA) antigen retrieval solution (AR0023, BOSTER Biological Technology Co., Ltd., Wuhan, China), 4 ′ ,6-diamidino-2-phenylindole (DAPI) staining solution (AR1176, BOSTER Biological Technology Co., Ltd., Wuhan, China), human TNF- α enzyme-linked immunosorbent assay (ELISA) kit (EK0525, BOSTER Biological Technology Co., Ltd., Wuhan, China), and human TGF- β 1 ELISA kit (EK0513, BOSTER Biological Technology Co., Ltd., Wuhan, China) were obtained from Boster, China.

Techniques: Inhibition, Staining, Modification, Comparison

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.

Techniques: Inhibition, Immunohistochemical staining, Staining

Inhibition of TNF- α reduced inflammation induced by glucose fluctuations in the aortic valves of diabetic rat models . (A,D) Immunostaining for TNF- α (indicated by arrows) revealed an elevated expression of the TNF- α protein in the aortic valves of the HG group, with an even greater upregulation observed in the GF group. Notably, the inhibition of TNF- α effectively reversed this upregulation in both the HG and GF groups. (B,E) The HG and GF groups exhibited an increased infiltration of CD3-positive T lymphocytes compared to the CTRL group; however, this increase could be mitigated by the inhibition of TNF- α . (C,F) The HG group showed increased CD68-positive macrophage infiltration compared to the CTRL group, and the GF group showed even higher levels; however, TNF- α inhibition could reduce this upregulation (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.

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 reduced inflammation induced by glucose fluctuations in the aortic valves of diabetic rat models . (A,D) Immunostaining for TNF- α (indicated by arrows) revealed an elevated expression of the TNF- α protein in the aortic valves of the HG group, with an even greater upregulation observed in the GF group. Notably, the inhibition of TNF- α effectively reversed this upregulation in both the HG and GF groups. (B,E) The HG and GF groups exhibited an increased infiltration of CD3-positive T lymphocytes compared to the CTRL group; however, this increase could be mitigated by the inhibition of TNF- α . (C,F) The HG group showed increased CD68-positive macrophage infiltration compared to the CTRL group, and the GF group showed even higher levels; however, TNF- α inhibition could reduce this upregulation (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.

Techniques: Inhibition, Immunostaining, Expressing

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.

Techniques: In Vitro, Expressing, Inhibition

TNF- α activated the JAK1/STAT3 pathway in vitro in porcine aortic valve interstitial cells under varying glucose concentrations . (A,B,E,F) In the pAVIC groups, both the HG and GF conditions upregulated the JAK1 protein expression. The presence of TNF- α exacerbated this upregulation under HG conditions, with a more pronounced effect observed under GF conditions. Conversely, the inhibition of TNF- α effectively reversed these upregulations in both the HG and GF groups. (C,D,G,H) In the pAVIC groups, phospho-STAT3 protein expression increased under both the HG and GF conditions, with TNF- α further enhancing this increase, especially in the GF conditions. Inhibiting TNF- α reversed these effects in both the HG and GF 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. JAK1, Janus kinase 1; STAT3, signal transducer and activator of transcription 3.

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 activated the JAK1/STAT3 pathway in vitro in porcine aortic valve interstitial cells under varying glucose concentrations . (A,B,E,F) In the pAVIC groups, both the HG and GF conditions upregulated the JAK1 protein expression. The presence of TNF- α exacerbated this upregulation under HG conditions, with a more pronounced effect observed under GF conditions. Conversely, the inhibition of TNF- α effectively reversed these upregulations in both the HG and GF groups. (C,D,G,H) In the pAVIC groups, phospho-STAT3 protein expression increased under both the HG and GF conditions, with TNF- α further enhancing this increase, especially in the GF conditions. Inhibiting TNF- α reversed these effects in both the HG and GF 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. JAK1, Janus kinase 1; STAT3, signal transducer and activator of transcription 3.

Techniques: In Vitro, Expressing, Inhibition

Inhibition of TNF- α led to the downregulation of the JAK1/STAT3 pathway in vivo in the aortic valves of diabetic rat models . (A,B) Immunohistochemical analysis of JAK1 (indicated by arrows) revealed an upregulation in JAK1 protein expression in the aortic valves of both HG and GF diabetic rat models. Notably, administration of infliximab was found to attenuate this upregulation. (C,D) Immunohistochemistry showed increased p-STAT3 protein expression in the aortic valves of the HG and GF diabetic rats, which was attenuated by the inhibition of TNF- α treatment. 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. B,D). * p < 0.05, scale bar = 100 µm.

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 led to the downregulation of the JAK1/STAT3 pathway in vivo in the aortic valves of diabetic rat models . (A,B) Immunohistochemical analysis of JAK1 (indicated by arrows) revealed an upregulation in JAK1 protein expression in the aortic valves of both HG and GF diabetic rat models. Notably, administration of infliximab was found to attenuate this upregulation. (C,D) Immunohistochemistry showed increased p-STAT3 protein expression in the aortic valves of the HG and GF diabetic rats, which was attenuated by the inhibition of TNF- α treatment. 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. B,D). * p < 0.05, scale bar = 100 µm.

Techniques: Inhibition, In Vivo, Immunohistochemical staining, Expressing, Immunohistochemistry

Colocalization of CD3, CD68, and JAK1 in the aortic valves of diabetic rat models . (A,B) The coimmunostaining analysis of the HG and GF groups demonstrated the presence of CD3, CD68, and JAK1 proteins, indicating that JAK1 expression is primarily localized in T lymphocytes and macrophages. Notably, this expression pattern could be altered through the inhibition of TNF- α . Scale bar = 50 µm. DAPI, 4 ′ ,6-diamidino-2-phenylindole.

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: Colocalization of CD3, CD68, and JAK1 in the aortic valves of diabetic rat models . (A,B) The coimmunostaining analysis of the HG and GF groups demonstrated the presence of CD3, CD68, and JAK1 proteins, indicating that JAK1 expression is primarily localized in T lymphocytes and macrophages. Notably, this expression pattern could be altered through the inhibition of TNF- α . Scale bar = 50 µm. DAPI, 4 ′ ,6-diamidino-2-phenylindole.

Techniques: Expressing, Inhibition

A working model of TNF- α -mediated JAK1/STAT3 pathway activation in glucose fluctuation-induced aortic valve fibrosis . GFs induce damage to VECs, which subsequently enhances the infiltration of macrophages and T lymphocytes, along with the secretion of TNF- α , and the activation of VICs. This cascade further augments the inflammatory signaling pathway, particularly through the upregulation of JAK1/STAT3. The phosphorylation of STAT3 facilitates its translocation into the nucleus, where it promotes the upregulation of fibrotic factors, thereby exacerbating the AVF. Red arrows: the specific proteins up-regulated.

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: A working model of TNF- α -mediated JAK1/STAT3 pathway activation in glucose fluctuation-induced aortic valve fibrosis . GFs induce damage to VECs, which subsequently enhances the infiltration of macrophages and T lymphocytes, along with the secretion of TNF- α , and the activation of VICs. This cascade further augments the inflammatory signaling pathway, particularly through the upregulation of JAK1/STAT3. The phosphorylation of STAT3 facilitates its translocation into the nucleus, where it promotes the upregulation of fibrotic factors, thereby exacerbating the AVF. Red arrows: the specific proteins up-regulated.

Techniques: Activation Assay, Phospho-proteomics, Translocation Assay

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