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Bioss col6a3
BIG improves cardiac function after I/RI by inhibiting the inflammatory response and myofibroblast fibrosis. (A, B, C, D, E, F, H and I) The relative expressions of MMP2, MMP9, TNF‒α, IL-1β, IL-6, BCL-2, BAX and c-caspase-3 (n=6). (G) WB results showing the expression of related proteins. (J) Representative microphotographs of TUNEL (blue, DAPI; green, TUNEL‒positive cardiomyocytes) staining of cardiomyocytes (n= 6). Scale bar: 20 μm. (K) The number of TUNEL‒positive cells represents the apoptosis rate in Sham, I/RI and BIG treated mice (n= 6). (L and M) The number of <t>Col6a3-</t> and TGF‒β‒positive myofibroblasts in the myocardial infarction area (n= 6). (N) Immunofluorescent colocalization of Col6a3, TGF‒β and vimentin in mice subjected to Sham, I/RI or BIG treatment (red, Col6a3 or TGF‒β; green, VIM; blue, DAPI). Scale bar: 50 μm. (O) Immunofluorescent colocalization of Col6a3, TGF‒β and TNNI3 in mice subjected to Sham, I/RI and BIG treatment (red, Col6a3 or TGF‒β; green, TNNI3; blue, DAPI). Scale bar: 50 μm. (P and Q) The number of Col6a3- and TGF‒β‒positive cardiomyocytes in the myocardial infarction area (n= 6). The data are presented as the means ± SEMs, and one-way ANOVA with Tukey’s multiple comparisons test was used for multiple groups comparisons, ***P < 0.001
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MedChemExpress recombinant endostatin
(A) Representative immunofluorescence images showing VEGF expression in the femoral head of control and SONFH groups (scale bar = 100 μm); (B) Quantification of VEGF fluorescence intensity in control and SONFH groups; (C) Representative immunofluorescence images showing <t>Endostatin</t> expression in the femoral head of control and SONFH groups (scale bar = 100 μm); (D) Quantification of Endostatin fluorescence intensity in these two groups; (E) Representative Western blotting images of MMP-2 expression in the femoral head of control and SONFH groups; (F) Quantification of MMP-2 expression in these two groups. (*P < 0.05, **P < 0.01).
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Bioss human collagen type ii alpha 1 col2a1 elisa kit
(A) Representative immunofluorescence images showing VEGF expression in the femoral head of control and SONFH groups (scale bar = 100 μm); (B) Quantification of VEGF fluorescence intensity in control and SONFH groups; (C) Representative immunofluorescence images showing <t>Endostatin</t> expression in the femoral head of control and SONFH groups (scale bar = 100 μm); (D) Quantification of Endostatin fluorescence intensity in these two groups; (E) Representative Western blotting images of MMP-2 expression in the femoral head of control and SONFH groups; (F) Quantification of MMP-2 expression in these two groups. (*P < 0.05, **P < 0.01).
Human Collagen Type Ii Alpha 1 Col2a1 Elisa Kit, supplied by Bioss, 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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MedChemExpress sonfh e ndostatin group
(A) Representative HE staining images of the femoral head in control, SONFH, <t>and</t> <t>SONFH+Endostatin</t> groups (scale bar = 100 μm); (B) Quantitative analysis of percentage of empty osteocyte from HE staining; (C) Representative micro-CT vascular reconstructions of the femoral head in each group; (D) Calcein staining images showing mineral apposition in each group (scale bar = 25 μm); (E) Quantitative analysis of vascular volume fraction from micro-CT angiography; (F) Quantification of mineral apposition rate (MAR) in each group. (*P < 0.05, ***P < 0.001, ****P < 0.0001).
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Bio-Techne corporation human pro-collagen i alpha 1 duoset elisa
(A) Representative HE staining images of the femoral head in control, SONFH, <t>and</t> <t>SONFH+Endostatin</t> groups (scale bar = 100 μm); (B) Quantitative analysis of percentage of empty osteocyte from HE staining; (C) Representative micro-CT vascular reconstructions of the femoral head in each group; (D) Calcein staining images showing mineral apposition in each group (scale bar = 25 μm); (E) Quantitative analysis of vascular volume fraction from micro-CT angiography; (F) Quantification of mineral apposition rate (MAR) in each group. (*P < 0.05, ***P < 0.001, ****P < 0.0001).
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Image Search Results


BIG improves cardiac function after I/RI by inhibiting the inflammatory response and myofibroblast fibrosis. (A, B, C, D, E, F, H and I) The relative expressions of MMP2, MMP9, TNF‒α, IL-1β, IL-6, BCL-2, BAX and c-caspase-3 (n=6). (G) WB results showing the expression of related proteins. (J) Representative microphotographs of TUNEL (blue, DAPI; green, TUNEL‒positive cardiomyocytes) staining of cardiomyocytes (n= 6). Scale bar: 20 μm. (K) The number of TUNEL‒positive cells represents the apoptosis rate in Sham, I/RI and BIG treated mice (n= 6). (L and M) The number of Col6a3- and TGF‒β‒positive myofibroblasts in the myocardial infarction area (n= 6). (N) Immunofluorescent colocalization of Col6a3, TGF‒β and vimentin in mice subjected to Sham, I/RI or BIG treatment (red, Col6a3 or TGF‒β; green, VIM; blue, DAPI). Scale bar: 50 μm. (O) Immunofluorescent colocalization of Col6a3, TGF‒β and TNNI3 in mice subjected to Sham, I/RI and BIG treatment (red, Col6a3 or TGF‒β; green, TNNI3; blue, DAPI). Scale bar: 50 μm. (P and Q) The number of Col6a3- and TGF‒β‒positive cardiomyocytes in the myocardial infarction area (n= 6). The data are presented as the means ± SEMs, and one-way ANOVA with Tukey’s multiple comparisons test was used for multiple groups comparisons, ***P < 0.001

Journal: Dose-Response

Article Title: 4,8-Dicarboxyl-8,9-Iridoid-1-Glycoside Alleviates Cardiac Dysfunction After Myocardial Ischaemia-Reperfusion Injury by Activating the PI3K/AKT Pathway

doi: 10.1177/15593258261444840

Figure Lengend Snippet: BIG improves cardiac function after I/RI by inhibiting the inflammatory response and myofibroblast fibrosis. (A, B, C, D, E, F, H and I) The relative expressions of MMP2, MMP9, TNF‒α, IL-1β, IL-6, BCL-2, BAX and c-caspase-3 (n=6). (G) WB results showing the expression of related proteins. (J) Representative microphotographs of TUNEL (blue, DAPI; green, TUNEL‒positive cardiomyocytes) staining of cardiomyocytes (n= 6). Scale bar: 20 μm. (K) The number of TUNEL‒positive cells represents the apoptosis rate in Sham, I/RI and BIG treated mice (n= 6). (L and M) The number of Col6a3- and TGF‒β‒positive myofibroblasts in the myocardial infarction area (n= 6). (N) Immunofluorescent colocalization of Col6a3, TGF‒β and vimentin in mice subjected to Sham, I/RI or BIG treatment (red, Col6a3 or TGF‒β; green, VIM; blue, DAPI). Scale bar: 50 μm. (O) Immunofluorescent colocalization of Col6a3, TGF‒β and TNNI3 in mice subjected to Sham, I/RI and BIG treatment (red, Col6a3 or TGF‒β; green, TNNI3; blue, DAPI). Scale bar: 50 μm. (P and Q) The number of Col6a3- and TGF‒β‒positive cardiomyocytes in the myocardial infarction area (n= 6). The data are presented as the means ± SEMs, and one-way ANOVA with Tukey’s multiple comparisons test was used for multiple groups comparisons, ***P < 0.001

Article Snippet: The blocking solution was removed, and the myocardial cells were treated with primary antibodies against TNNI3 (1:50) (Bioss, BD-PE0227), Col6a3 (1:100) (Bioss, bs-0553R), and TGF-β (1:200) (Affinity, AF1027); the myocardial fibroblasts were then treated with primary antibodies against vimentin (1:100) (Bioss, BD-PE1985), Col6a3 (1:100), and TGF-β (1:200).

Techniques: Expressing, TUNEL Assay, Staining

Changes in the multiomic map after myocardial infarction. (A) UMAP of the snRNA‒seq data from all the samples (n = 191,795). (B) Differential expression of Col6a3 in cardiac fibroblasts (n = 47,309) and cardiomyocytes (n = 64,510). (C) Volcano plot of the expression of all genes in myocardial fibroblasts and cardiomyocytes in the infarct area. Red, upregulated; green, downregulated; grey, no difference. (D) KEGG of differentially expressed genes. (E) The expressions of Col6a3 and TGF‒β in the myocardial tissue of the infarct area in the Sham, I/RI, and BIG treated mice (n = 6). The data are presented as the means ± SEMs, and one-way ANOVA with Tukey’s multiple comparisons test was used for multiple groups comparisons, ***P < 0.001

Journal: Dose-Response

Article Title: 4,8-Dicarboxyl-8,9-Iridoid-1-Glycoside Alleviates Cardiac Dysfunction After Myocardial Ischaemia-Reperfusion Injury by Activating the PI3K/AKT Pathway

doi: 10.1177/15593258261444840

Figure Lengend Snippet: Changes in the multiomic map after myocardial infarction. (A) UMAP of the snRNA‒seq data from all the samples (n = 191,795). (B) Differential expression of Col6a3 in cardiac fibroblasts (n = 47,309) and cardiomyocytes (n = 64,510). (C) Volcano plot of the expression of all genes in myocardial fibroblasts and cardiomyocytes in the infarct area. Red, upregulated; green, downregulated; grey, no difference. (D) KEGG of differentially expressed genes. (E) The expressions of Col6a3 and TGF‒β in the myocardial tissue of the infarct area in the Sham, I/RI, and BIG treated mice (n = 6). The data are presented as the means ± SEMs, and one-way ANOVA with Tukey’s multiple comparisons test was used for multiple groups comparisons, ***P < 0.001

Article Snippet: The blocking solution was removed, and the myocardial cells were treated with primary antibodies against TNNI3 (1:50) (Bioss, BD-PE0227), Col6a3 (1:100) (Bioss, bs-0553R), and TGF-β (1:200) (Affinity, AF1027); the myocardial fibroblasts were then treated with primary antibodies against vimentin (1:100) (Bioss, BD-PE1985), Col6a3 (1:100), and TGF-β (1:200).

Techniques: Quantitative Proteomics, Expressing

(A) Representative immunofluorescence images showing VEGF expression in the femoral head of control and SONFH groups (scale bar = 100 μm); (B) Quantification of VEGF fluorescence intensity in control and SONFH groups; (C) Representative immunofluorescence images showing Endostatin expression in the femoral head of control and SONFH groups (scale bar = 100 μm); (D) Quantification of Endostatin fluorescence intensity in these two groups; (E) Representative Western blotting images of MMP-2 expression in the femoral head of control and SONFH groups; (F) Quantification of MMP-2 expression in these two groups. (*P < 0.05, **P < 0.01).

Journal: PLOS One

Article Title: MMP-2 associated imbalance of VEGF/Endostatin is linked to suppression of the PI3K/AKT/HIF-1α pathway in steroid-induced osteonecrosis of femoral head

doi: 10.1371/journal.pone.0346880

Figure Lengend Snippet: (A) Representative immunofluorescence images showing VEGF expression in the femoral head of control and SONFH groups (scale bar = 100 μm); (B) Quantification of VEGF fluorescence intensity in control and SONFH groups; (C) Representative immunofluorescence images showing Endostatin expression in the femoral head of control and SONFH groups (scale bar = 100 μm); (D) Quantification of Endostatin fluorescence intensity in these two groups; (E) Representative Western blotting images of MMP-2 expression in the femoral head of control and SONFH groups; (F) Quantification of MMP-2 expression in these two groups. (*P < 0.05, **P < 0.01).

Article Snippet: Mice in the SONFH+MMP-2 group received subcutaneous injections of recombinant MMP-2 (10 μg/kg; MedChemExpress, NJ, USA) every three days [ , ], while those in the SONFH+Endostatin group were administered daily subcutaneous injections of recombinant Endostatin (2 mg/kg; MedChemExpress, NJ, USA) [ ].

Techniques: Immunofluorescence, Expressing, Control, Fluorescence, Western Blot

(A) Representative HE staining images of the femoral head in control, SONFH, and SONFH+Endostatin groups (scale bar = 100 μm); (B) Quantitative analysis of percentage of empty osteocyte from HE staining; (C) Representative micro-CT vascular reconstructions of the femoral head in each group; (D) Calcein staining images showing mineral apposition in each group (scale bar = 25 μm); (E) Quantitative analysis of vascular volume fraction from micro-CT angiography; (F) Quantification of mineral apposition rate (MAR) in each group. (*P < 0.05, ***P < 0.001, ****P < 0.0001).

Journal: PLOS One

Article Title: MMP-2 associated imbalance of VEGF/Endostatin is linked to suppression of the PI3K/AKT/HIF-1α pathway in steroid-induced osteonecrosis of femoral head

doi: 10.1371/journal.pone.0346880

Figure Lengend Snippet: (A) Representative HE staining images of the femoral head in control, SONFH, and SONFH+Endostatin groups (scale bar = 100 μm); (B) Quantitative analysis of percentage of empty osteocyte from HE staining; (C) Representative micro-CT vascular reconstructions of the femoral head in each group; (D) Calcein staining images showing mineral apposition in each group (scale bar = 25 μm); (E) Quantitative analysis of vascular volume fraction from micro-CT angiography; (F) Quantification of mineral apposition rate (MAR) in each group. (*P < 0.05, ***P < 0.001, ****P < 0.0001).

Article Snippet: Mice in the SONFH+MMP-2 group received subcutaneous injections of recombinant MMP-2 (10 μg/kg; MedChemExpress, NJ, USA) every three days [ , ], while those in the SONFH+Endostatin group were administered daily subcutaneous injections of recombinant Endostatin (2 mg/kg; MedChemExpress, NJ, USA) [ ].

Techniques: Staining, Control, Micro-CT

(A) Relative mRNA levels of Endostatin in the femoral head tissues of each group; (B) Western blotting images showing Endostatin protein expression; (C) Quantification of Endostatin protein levels; (D) Representative immunofluorescence images of Endostatin expression; (E) Quantitative analysis of Endostatin immunofluorescence intensity. (*P < 0.05, **P < 0.01, ***P < 0.001).

Journal: PLOS One

Article Title: MMP-2 associated imbalance of VEGF/Endostatin is linked to suppression of the PI3K/AKT/HIF-1α pathway in steroid-induced osteonecrosis of femoral head

doi: 10.1371/journal.pone.0346880

Figure Lengend Snippet: (A) Relative mRNA levels of Endostatin in the femoral head tissues of each group; (B) Western blotting images showing Endostatin protein expression; (C) Quantification of Endostatin protein levels; (D) Representative immunofluorescence images of Endostatin expression; (E) Quantitative analysis of Endostatin immunofluorescence intensity. (*P < 0.05, **P < 0.01, ***P < 0.001).

Article Snippet: Mice in the SONFH+MMP-2 group received subcutaneous injections of recombinant MMP-2 (10 μg/kg; MedChemExpress, NJ, USA) every three days [ , ], while those in the SONFH+Endostatin group were administered daily subcutaneous injections of recombinant Endostatin (2 mg/kg; MedChemExpress, NJ, USA) [ ].

Techniques: Western Blot, Expressing, Immunofluorescence

(A) Representative HE staining images of the femoral head in control, SONFH, and SONFH+Endostatin groups (scale bar = 100 μm); (B) Quantitative analysis of percentage of empty osteocyte from HE staining; (C) Representative micro-CT vascular reconstructions of the femoral head in each group; (D) Calcein staining images showing mineral apposition in each group (scale bar = 25 μm); (E) Quantitative analysis of vascular volume fraction from micro-CT angiography; (F) Quantification of mineral apposition rate (MAR) in each group. (*P < 0.05, ***P < 0.001, ****P < 0.0001).

Journal: PLOS One

Article Title: MMP-2 associated imbalance of VEGF/Endostatin is linked to suppression of the PI3K/AKT/HIF-1α pathway in steroid-induced osteonecrosis of femoral head

doi: 10.1371/journal.pone.0346880

Figure Lengend Snippet: (A) Representative HE staining images of the femoral head in control, SONFH, and SONFH+Endostatin groups (scale bar = 100 μm); (B) Quantitative analysis of percentage of empty osteocyte from HE staining; (C) Representative micro-CT vascular reconstructions of the femoral head in each group; (D) Calcein staining images showing mineral apposition in each group (scale bar = 25 μm); (E) Quantitative analysis of vascular volume fraction from micro-CT angiography; (F) Quantification of mineral apposition rate (MAR) in each group. (*P < 0.05, ***P < 0.001, ****P < 0.0001).

Article Snippet: Mice in the SONFH+MMP-2 group received subcutaneous injections of recombinant MMP-2 (10 μg/kg; MedChemExpress, NJ, USA) every three days [ , ], while those in the SONFH+Endostatin group were administered daily subcutaneous injections of recombinant Endostatin (2 mg/kg; MedChemExpress, NJ, USA) [ ].

Techniques: Staining, Control, Micro-CT