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mouse col1 elisa kit  (Elabscience Biotechnology)


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    Elabscience Biotechnology mouse col1 elisa kit
    Mouse Col1 Elisa Kit, supplied by Elabscience Biotechnology, used in various techniques. Bioz Stars score: 94/100, based on 19 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/mouse+col1+elisa+kit/pm41679474-51-0-7?v=Elabscience+Biotechnology
    Average 94 stars, based on 19 article reviews
    mouse col1 elisa kit - by Bioz Stars, 2026-07
    94/100 stars

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    Preparation and characterization of RGD@LP-Y. ( A ) Schematic illustration of RGD@LP-Y preparation. ( B ) TEM observation of RGD@LP-Y morphology. ( C ) Zeta potential of RGD@LP-Y. ( D ) The cumulative release of LP-Y and RGD@LP-Y at different pH values (pH 7.4 and 5.5). ( E ) Variations in the particle size of RGD@LP-Y under conditions of 4 ℃, -20 ℃, -80 ℃, and 10% serum after 12 days. ( F ) Relative viability of Hepa1-6 cells treated with different liposomes measured by CCK-8 assay. ( G ) mRNA expression levels of YAP and <t>COL1A2.</t> ( F ) Detection of <t>COL1</t> level in Hepa1-6 cell supernatant by ELISA. LP, liposomes without RGD modification; RGD@LP, RGD-modified liposomes; LP-Y, liposomes encapsulating Y-27632 but without RGD modification; RGD@LP-Y, RGD-modified liposomes encapsulated with Y-27632. Values represent mean±SD. *P < 0.05, **P < 0.01, ***P < 0.001. ns: not significant.
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    Preparation and characterization of RGD@LP-Y. ( A ) Schematic illustration of RGD@LP-Y preparation. ( B ) TEM observation of RGD@LP-Y morphology. ( C ) Zeta potential of RGD@LP-Y. ( D ) The cumulative release of LP-Y and RGD@LP-Y at different pH values (pH 7.4 and 5.5). ( E ) Variations in the particle size of RGD@LP-Y under conditions of 4 ℃, -20 ℃, -80 ℃, and 10% serum after 12 days. ( F ) Relative viability of Hepa1-6 cells treated with different liposomes measured by CCK-8 assay. ( G ) mRNA expression levels of YAP and <t>COL1A2.</t> ( F ) Detection of <t>COL1</t> level in Hepa1-6 cell supernatant by ELISA. LP, liposomes without RGD modification; RGD@LP, RGD-modified liposomes; LP-Y, liposomes encapsulating Y-27632 but without RGD modification; RGD@LP-Y, RGD-modified liposomes encapsulated with Y-27632. Values represent mean±SD. *P < 0.05, **P < 0.01, ***P < 0.001. ns: not significant.
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    Fig. 6 The regulatory effect of P2X7 receptor via the PI3K/AKT/GSK3β signaling pathway in vivo. A Western blot analysis measured the phosphorylation levels and grayscale values of P13K, AKT, and GSK3β proteins in mouse femur tissue from each group; B immunohistochemistry staining assessed the expression and positive area percentage of p-P13K, p-AKT, and p-GSK3β in mouse femur tissue of each group; C bar graph presenting the number of TRAP-positive cells in mouse femur tissue sections stained with TRAP; D western blot analysis determined the expression levels and band grayscale values of MMP9, NFATc1, and CK proteins in mouse femur tissue from each group; E immunohistochemistry staining assessed the expression and positive area percentage of MMP9 and NFATc1 in mouse femur tissue; F <t>ELISA</t> measured the expression levels of CTX and <t>NTX</t> in mouse serum; G Von Kossa staining assessed the calcium salt deposition in mouse femur tissue sections. Bar = 100 μm. Compared with the WT + Sham group, ***P < 0.001; compared with the WT + OVX group, ###P < 0.001; compared with the KO + OVX group, &&&P < 0.001
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    SHH promoted collagen deposition and polarization of M2 macrophage. A , wound model of dorsal skin was established in C57BL/6 mice, and the wound was treated with rmSHH or vector. The wound size during the healing period was recorded and measured ( n = 6). B , masson staining was performed and the dermal layer were measured to evaluate the collagen deposition of the wound bed. C , <t>ELISA</t> was performed to measure the expression of <t>type</t> <t>I</t> <t>collagen</t> of the wound. D , IHC of CD31 was performed to compared the neovascularization of the two group. E-G , IF of Ly6G, F4/80, iNOS and CD206 were performed to evaluate the infiltration of neutrophil (E) , M1 (F) and M2 macrophage (G) . H , flow cytometry was performed to evaluate the macrophage phenotype of the wound bed. * p < 0.05, ** p < 0.01, n = 6
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    SHH promoted collagen deposition and polarization of M2 macrophage. A , wound model of dorsal skin was established in C57BL/6 mice, and the wound was treated with rmSHH or vector. The wound size during the healing period was recorded and measured ( n = 6). B , masson staining was performed and the dermal layer were measured to evaluate the collagen deposition of the wound bed. C , <t>ELISA</t> was performed to measure the expression of <t>type</t> <t>I</t> <t>collagen</t> of the wound. D , IHC of CD31 was performed to compared the neovascularization of the two group. E-G , IF of Ly6G, F4/80, iNOS and CD206 were performed to evaluate the infiltration of neutrophil (E) , M1 (F) and M2 macrophage (G) . H , flow cytometry was performed to evaluate the macrophage phenotype of the wound bed. * p < 0.05, ** p < 0.01, n = 6
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    SHH promoted collagen deposition and polarization of M2 macrophage. A , wound model of dorsal skin was established in C57BL/6 mice, and the wound was treated with rmSHH or vector. The wound size during the healing period was recorded and measured ( n = 6). B , masson staining was performed and the dermal layer were measured to evaluate the collagen deposition of the wound bed. C , <t>ELISA</t> was performed to measure the expression of <t>type</t> <t>I</t> <t>collagen</t> of the wound. D , IHC of CD31 was performed to compared the neovascularization of the two group. E-G , IF of Ly6G, F4/80, iNOS and CD206 were performed to evaluate the infiltration of neutrophil (E) , M1 (F) and M2 macrophage (G) . H , flow cytometry was performed to evaluate the macrophage phenotype of the wound bed. * p < 0.05, ** p < 0.01, n = 6
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    Image Search Results


    Preparation and characterization of RGD@LP-Y. ( A ) Schematic illustration of RGD@LP-Y preparation. ( B ) TEM observation of RGD@LP-Y morphology. ( C ) Zeta potential of RGD@LP-Y. ( D ) The cumulative release of LP-Y and RGD@LP-Y at different pH values (pH 7.4 and 5.5). ( E ) Variations in the particle size of RGD@LP-Y under conditions of 4 ℃, -20 ℃, -80 ℃, and 10% serum after 12 days. ( F ) Relative viability of Hepa1-6 cells treated with different liposomes measured by CCK-8 assay. ( G ) mRNA expression levels of YAP and COL1A2. ( F ) Detection of COL1 level in Hepa1-6 cell supernatant by ELISA. LP, liposomes without RGD modification; RGD@LP, RGD-modified liposomes; LP-Y, liposomes encapsulating Y-27632 but without RGD modification; RGD@LP-Y, RGD-modified liposomes encapsulated with Y-27632. Values represent mean±SD. *P < 0.05, **P < 0.01, ***P < 0.001. ns: not significant.

    Journal: Theranostics

    Article Title: Nanodelivery of Y-27632 by RGD-modified liposome enhances radioimmunotherapy of hepatocellular carcinoma via tumor microenvironment matrix stiffness reprogramming

    doi: 10.7150/thno.114892

    Figure Lengend Snippet: Preparation and characterization of RGD@LP-Y. ( A ) Schematic illustration of RGD@LP-Y preparation. ( B ) TEM observation of RGD@LP-Y morphology. ( C ) Zeta potential of RGD@LP-Y. ( D ) The cumulative release of LP-Y and RGD@LP-Y at different pH values (pH 7.4 and 5.5). ( E ) Variations in the particle size of RGD@LP-Y under conditions of 4 ℃, -20 ℃, -80 ℃, and 10% serum after 12 days. ( F ) Relative viability of Hepa1-6 cells treated with different liposomes measured by CCK-8 assay. ( G ) mRNA expression levels of YAP and COL1A2. ( F ) Detection of COL1 level in Hepa1-6 cell supernatant by ELISA. LP, liposomes without RGD modification; RGD@LP, RGD-modified liposomes; LP-Y, liposomes encapsulating Y-27632 but without RGD modification; RGD@LP-Y, RGD-modified liposomes encapsulated with Y-27632. Values represent mean±SD. *P < 0.05, **P < 0.01, ***P < 0.001. ns: not significant.

    Article Snippet: The Mouse IL-12 (Interleukin 12) ELISA Kit [E-EL-M3062], Mouse COL1 (Collagen Type I) ELISA Kit[E-EL-M0325], Human TNF-α (Tumor Necrosis Factor Alpha) ELISA Kit [E-EL-H0109], Human IL-6 (Interleukin 6) ELISA Kit [E-EL-H6156], Human IL-1β (Interleukin 1 Beta) ELISA Kit [E-EL-H0149], Mouse IL-6 (Interleukin 6) ELISA Kit [E-EL-M0044], and Mouse TNF-α (Tumor Necrosis Factor Alpha) ELISA Kit [E-EL-M3063] were purchased from Elabscience Biotechnology Co., Ltd. (China).

    Techniques: Zeta Potential Analyzer, Liposomes, CCK-8 Assay, Expressing, Enzyme-linked Immunosorbent Assay, Modification

    Fig. 6 The regulatory effect of P2X7 receptor via the PI3K/AKT/GSK3β signaling pathway in vivo. A Western blot analysis measured the phosphorylation levels and grayscale values of P13K, AKT, and GSK3β proteins in mouse femur tissue from each group; B immunohistochemistry staining assessed the expression and positive area percentage of p-P13K, p-AKT, and p-GSK3β in mouse femur tissue of each group; C bar graph presenting the number of TRAP-positive cells in mouse femur tissue sections stained with TRAP; D western blot analysis determined the expression levels and band grayscale values of MMP9, NFATc1, and CK proteins in mouse femur tissue from each group; E immunohistochemistry staining assessed the expression and positive area percentage of MMP9 and NFATc1 in mouse femur tissue; F ELISA measured the expression levels of CTX and NTX in mouse serum; G Von Kossa staining assessed the calcium salt deposition in mouse femur tissue sections. Bar = 100 μm. Compared with the WT + Sham group, ***P < 0.001; compared with the WT + OVX group, ###P < 0.001; compared with the KO + OVX group, &&&P < 0.001

    Journal: Cellular & molecular biology letters

    Article Title: New mechanistic understanding of osteoclast differentiation and bone resorption mediated by P2X7 receptors and PI3K-Akt-GSK3β signaling.

    doi: 10.1186/s11658-024-00614-5

    Figure Lengend Snippet: Fig. 6 The regulatory effect of P2X7 receptor via the PI3K/AKT/GSK3β signaling pathway in vivo. A Western blot analysis measured the phosphorylation levels and grayscale values of P13K, AKT, and GSK3β proteins in mouse femur tissue from each group; B immunohistochemistry staining assessed the expression and positive area percentage of p-P13K, p-AKT, and p-GSK3β in mouse femur tissue of each group; C bar graph presenting the number of TRAP-positive cells in mouse femur tissue sections stained with TRAP; D western blot analysis determined the expression levels and band grayscale values of MMP9, NFATc1, and CK proteins in mouse femur tissue from each group; E immunohistochemistry staining assessed the expression and positive area percentage of MMP9 and NFATc1 in mouse femur tissue; F ELISA measured the expression levels of CTX and NTX in mouse serum; G Von Kossa staining assessed the calcium salt deposition in mouse femur tissue sections. Bar = 100 μm. Compared with the WT + Sham group, ***P < 0.001; compared with the WT + OVX group, ###P < 0.001; compared with the KO + OVX group, &&&P < 0.001

    Article Snippet: We used a mouse Cross-linked Type I Collagen C-Telopeptide (CTX) ELISA kit (M3023, Elabscience, Wuhan, China) and a mouse Cross-linked Type I Collagen N-Telopeptide (NTX) ELISA kit (E-EL-M3022, Elabscience, Wuhan, China) for mice.

    Techniques: In Vivo, Western Blot, Phospho-proteomics, Immunohistochemistry, Staining, Expressing, Enzyme-linked Immunosorbent Assay

    SHH promoted collagen deposition and polarization of M2 macrophage. A , wound model of dorsal skin was established in C57BL/6 mice, and the wound was treated with rmSHH or vector. The wound size during the healing period was recorded and measured ( n = 6). B , masson staining was performed and the dermal layer were measured to evaluate the collagen deposition of the wound bed. C , ELISA was performed to measure the expression of type I collagen of the wound. D , IHC of CD31 was performed to compared the neovascularization of the two group. E-G , IF of Ly6G, F4/80, iNOS and CD206 were performed to evaluate the infiltration of neutrophil (E) , M1 (F) and M2 macrophage (G) . H , flow cytometry was performed to evaluate the macrophage phenotype of the wound bed. * p < 0.05, ** p < 0.01, n = 6

    Journal: Cell Communication and Signaling : CCS

    Article Title: SHH induces macrophage oxidative phosphorylation and efferocytosis to promote scar formation

    doi: 10.1186/s12964-024-01692-w

    Figure Lengend Snippet: SHH promoted collagen deposition and polarization of M2 macrophage. A , wound model of dorsal skin was established in C57BL/6 mice, and the wound was treated with rmSHH or vector. The wound size during the healing period was recorded and measured ( n = 6). B , masson staining was performed and the dermal layer were measured to evaluate the collagen deposition of the wound bed. C , ELISA was performed to measure the expression of type I collagen of the wound. D , IHC of CD31 was performed to compared the neovascularization of the two group. E-G , IF of Ly6G, F4/80, iNOS and CD206 were performed to evaluate the infiltration of neutrophil (E) , M1 (F) and M2 macrophage (G) . H , flow cytometry was performed to evaluate the macrophage phenotype of the wound bed. * p < 0.05, ** p < 0.01, n = 6

    Article Snippet: Mouse COL1 ELISA Kit (No.D721060, Sangon Biotech, China) was used for COL1 determination of the wound area.

    Techniques: Plasmid Preparation, Staining, Enzyme-linked Immunosorbent Assay, Expressing, Flow Cytometry

    Vismodegib alleviated scar formation by targeting SHH signal. A-D , OCR, maximal respiration response, complex I, II and ATP production of macrophage treated with vismodegib were measured ( n = 3). E , apoptotic neutrophil was marked with PKH26 and incubated with bone marrow derived macrophage. Flow cytometry was performed to evaluate the efferocytosis of macrophage treated with vismodegib ( n = 3). F-J , wound model of dorsal skin was established in C57BL/6 mice, and vismodegib was administrated ( n = 6). F , masson staining was performed and the dermal layer were measured to evaluate the collagen deposition of the wound bed. G , IF and ELISA was performed to evaluate the expression of type I collagen. H-I , IF of F4/80, iNOS and CD206 were performed to evaluate the macrophage infiltration of wound bed. J , flow cytometry was performed to evaluate the phenotype of macrophage from wound bed treated with vismodegib. * p < 0.05, ** p < 0.01

    Journal: Cell Communication and Signaling : CCS

    Article Title: SHH induces macrophage oxidative phosphorylation and efferocytosis to promote scar formation

    doi: 10.1186/s12964-024-01692-w

    Figure Lengend Snippet: Vismodegib alleviated scar formation by targeting SHH signal. A-D , OCR, maximal respiration response, complex I, II and ATP production of macrophage treated with vismodegib were measured ( n = 3). E , apoptotic neutrophil was marked with PKH26 and incubated with bone marrow derived macrophage. Flow cytometry was performed to evaluate the efferocytosis of macrophage treated with vismodegib ( n = 3). F-J , wound model of dorsal skin was established in C57BL/6 mice, and vismodegib was administrated ( n = 6). F , masson staining was performed and the dermal layer were measured to evaluate the collagen deposition of the wound bed. G , IF and ELISA was performed to evaluate the expression of type I collagen. H-I , IF of F4/80, iNOS and CD206 were performed to evaluate the macrophage infiltration of wound bed. J , flow cytometry was performed to evaluate the phenotype of macrophage from wound bed treated with vismodegib. * p < 0.05, ** p < 0.01

    Article Snippet: Mouse COL1 ELISA Kit (No.D721060, Sangon Biotech, China) was used for COL1 determination of the wound area.

    Techniques: Incubation, Derivative Assay, Flow Cytometry, Staining, Enzyme-linked Immunosorbent Assay, Expressing