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rabbit anti mouse a sma  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc rabbit anti mouse a sma
    Rabbit Anti Mouse A Sma, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 257 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/rabbit anti mouse a sma/product/Cell Signaling Technology Inc
    Average 96 stars, based on 257 article reviews
    rabbit anti mouse a sma - by Bioz Stars, 2026-02
    96/100 stars

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    Proteintech primary antibodies include rabbit anti mouse α sma antibody
    Figure 3. Cep induced liver damage. A, Serum levels of AST and ALT in Apoe−/− and Ldlr−/− mice treated with or without Cep. n = 9 for each group in Apoe−/− mice; n = 8 for the Veh group and n = 6 for the Cep group in Ldlr−/− mice; B, Gross images of liver from Apoe−/− and Ldlr−/− mice treated with or without Cep. n = 6 for the Veh group and n = 7 for the Cep group in Apoe−/− mice; n = 8 for the Veh group and n = 6 for the Cep group in Ldlr−/− mice. Scale bar: 1 cm; C, Liver weight and liver weight index in Apoe−/− and Ldlr−/− mice treated with or without Cep; D, H&E staining of livers from Apoe−/− and Ldlr−/− mice treated with or without Cep. Both internal and peripheral liver sections were captured. n = 9 for the Veh group and n = 8 for the Cep group in Apoe−/− mice; n = 7 for the Veh group and n = 6 for the Cep group in Ldlr−/− mice. Scale bar: 20 μm; E, Sirius red staining of liver sections from Apoe−/− and Ldlr−/− mice treated with or without Cep. Internal and peripheral liver sections were captured. Scale bar: 50 μm; F, Immunofluorescence staining of COL1A1 in liver sections from Apoe−/− and Ldlr−/− mice. Scale bar: 50 μm. n = 5 for each group; G, Immunofluorescence staining <t>of</t> <t>α-SMA</t> in liver sections from Apoe−/− and Ldlr−/− mice liver. Scale bar: 100 μm. n = 5 for each group. All data are presented as the means ± SD. Data for ALT in Apoe−/− mice, and AST and ALT in Ldlr−/− mice were analyzed using the Kolmogorov- Smirnov test. Data for AST in Apoe−/− mice were analyzed using an unpaired Student t test. For C, liver weight in Apoe−/− mice was analyzed using the Kolmogorov-Smirnov test; liver weight index in Apoe−/− mice, and liver weight and liver weight index in Ldlr−/− mice were analyzed using an unpaired Student t test. ALT: alanine aminotransferase; AST: aspartate aminotransferase; Cep: cepharanthine; COL1A1: collagen type I alpha 1; DAPI: 4’-6-diamidino-2- phenylindole; H&E: hematoxylin and eosin; SD: standard <t>deviation;</t> <t>α-SMA:</t> alpha-smooth muscle actin; Veh: vehicle.
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    Cell Signaling Technology Inc resource source identifier rabbit anti-mouse a-sma antibody cell signaling cell signaling: cat# 19245
    Figure 3. Cep induced liver damage. A, Serum levels of AST and ALT in Apoe−/− and Ldlr−/− mice treated with or without Cep. n = 9 for each group in Apoe−/− mice; n = 8 for the Veh group and n = 6 for the Cep group in Ldlr−/− mice; B, Gross images of liver from Apoe−/− and Ldlr−/− mice treated with or without Cep. n = 6 for the Veh group and n = 7 for the Cep group in Apoe−/− mice; n = 8 for the Veh group and n = 6 for the Cep group in Ldlr−/− mice. Scale bar: 1 cm; C, Liver weight and liver weight index in Apoe−/− and Ldlr−/− mice treated with or without Cep; D, H&E staining of livers from Apoe−/− and Ldlr−/− mice treated with or without Cep. Both internal and peripheral liver sections were captured. n = 9 for the Veh group and n = 8 for the Cep group in Apoe−/− mice; n = 7 for the Veh group and n = 6 for the Cep group in Ldlr−/− mice. Scale bar: 20 μm; E, Sirius red staining of liver sections from Apoe−/− and Ldlr−/− mice treated with or without Cep. Internal and peripheral liver sections were captured. Scale bar: 50 μm; F, Immunofluorescence staining of COL1A1 in liver sections from Apoe−/− and Ldlr−/− mice. Scale bar: 50 μm. n = 5 for each group; G, Immunofluorescence staining <t>of</t> <t>α-SMA</t> in liver sections from Apoe−/− and Ldlr−/− mice liver. Scale bar: 100 μm. n = 5 for each group. All data are presented as the means ± SD. Data for ALT in Apoe−/− mice, and AST and ALT in Ldlr−/− mice were analyzed using the Kolmogorov- Smirnov test. Data for AST in Apoe−/− mice were analyzed using an unpaired Student t test. For C, liver weight in Apoe−/− mice was analyzed using the Kolmogorov-Smirnov test; liver weight index in Apoe−/− mice, and liver weight and liver weight index in Ldlr−/− mice were analyzed using an unpaired Student t test. ALT: alanine aminotransferase; AST: aspartate aminotransferase; Cep: cepharanthine; COL1A1: collagen type I alpha 1; DAPI: 4’-6-diamidino-2- phenylindole; H&E: hematoxylin and eosin; SD: standard <t>deviation;</t> <t>α-SMA:</t> alpha-smooth muscle actin; Veh: vehicle.
    Resource Source Identifier Rabbit Anti Mouse A Sma Antibody Cell Signaling Cell Signaling: Cat# 19245, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Figure 3. Cep induced liver damage. A, Serum levels of AST and ALT in Apoe−/− and Ldlr−/− mice treated with or without Cep. n = 9 for each group in Apoe−/− mice; n = 8 for the Veh group and n = 6 for the Cep group in Ldlr−/− mice; B, Gross images of liver from Apoe−/− and Ldlr−/− mice treated with or without Cep. n = 6 for the Veh group and n = 7 for the Cep group in Apoe−/− mice; n = 8 for the Veh group and n = 6 for the Cep group in Ldlr−/− mice. Scale bar: 1 cm; C, Liver weight and liver weight index in Apoe−/− and Ldlr−/− mice treated with or without Cep; D, H&E staining of livers from Apoe−/− and Ldlr−/− mice treated with or without Cep. Both internal and peripheral liver sections were captured. n = 9 for the Veh group and n = 8 for the Cep group in Apoe−/− mice; n = 7 for the Veh group and n = 6 for the Cep group in Ldlr−/− mice. Scale bar: 20 μm; E, Sirius red staining of liver sections from Apoe−/− and Ldlr−/− mice treated with or without Cep. Internal and peripheral liver sections were captured. Scale bar: 50 μm; F, Immunofluorescence staining of COL1A1 in liver sections from Apoe−/− and Ldlr−/− mice. Scale bar: 50 μm. n = 5 for each group; G, Immunofluorescence staining <t>of</t> <t>α-SMA</t> in liver sections from Apoe−/− and Ldlr−/− mice liver. Scale bar: 100 μm. n = 5 for each group. All data are presented as the means ± SD. Data for ALT in Apoe−/− mice, and AST and ALT in Ldlr−/− mice were analyzed using the Kolmogorov- Smirnov test. Data for AST in Apoe−/− mice were analyzed using an unpaired Student t test. For C, liver weight in Apoe−/− mice was analyzed using the Kolmogorov-Smirnov test; liver weight index in Apoe−/− mice, and liver weight and liver weight index in Ldlr−/− mice were analyzed using an unpaired Student t test. ALT: alanine aminotransferase; AST: aspartate aminotransferase; Cep: cepharanthine; COL1A1: collagen type I alpha 1; DAPI: 4’-6-diamidino-2- phenylindole; H&E: hematoxylin and eosin; SD: standard <t>deviation;</t> <t>α-SMA:</t> alpha-smooth muscle actin; Veh: vehicle.
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    Figure 3. Cep induced liver damage. A, Serum levels of AST and ALT in Apoe−/− and Ldlr−/− mice treated with or without Cep. n = 9 for each group in Apoe−/− mice; n = 8 for the Veh group and n = 6 for the Cep group in Ldlr−/− mice; B, Gross images of liver from Apoe−/− and Ldlr−/− mice treated with or without Cep. n = 6 for the Veh group and n = 7 for the Cep group in Apoe−/− mice; n = 8 for the Veh group and n = 6 for the Cep group in Ldlr−/− mice. Scale bar: 1 cm; C, Liver weight and liver weight index in Apoe−/− and Ldlr−/− mice treated with or without Cep; D, H&E staining of livers from Apoe−/− and Ldlr−/− mice treated with or without Cep. Both internal and peripheral liver sections were captured. n = 9 for the Veh group and n = 8 for the Cep group in Apoe−/− mice; n = 7 for the Veh group and n = 6 for the Cep group in Ldlr−/− mice. Scale bar: 20 μm; E, Sirius red staining of liver sections from Apoe−/− and Ldlr−/− mice treated with or without Cep. Internal and peripheral liver sections were captured. Scale bar: 50 μm; F, Immunofluorescence staining of COL1A1 in liver sections from Apoe−/− and Ldlr−/− mice. Scale bar: 50 μm. n = 5 for each group; G, Immunofluorescence staining <t>of</t> <t>α-SMA</t> in liver sections from Apoe−/− and Ldlr−/− mice liver. Scale bar: 100 μm. n = 5 for each group. All data are presented as the means ± SD. Data for ALT in Apoe−/− mice, and AST and ALT in Ldlr−/− mice were analyzed using the Kolmogorov- Smirnov test. Data for AST in Apoe−/− mice were analyzed using an unpaired Student t test. For C, liver weight in Apoe−/− mice was analyzed using the Kolmogorov-Smirnov test; liver weight index in Apoe−/− mice, and liver weight and liver weight index in Ldlr−/− mice were analyzed using an unpaired Student t test. ALT: alanine aminotransferase; AST: aspartate aminotransferase; Cep: cepharanthine; COL1A1: collagen type I alpha 1; DAPI: 4’-6-diamidino-2- phenylindole; H&E: hematoxylin and eosin; SD: standard <t>deviation;</t> <t>α-SMA:</t> alpha-smooth muscle actin; Veh: vehicle.
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    Servicebio Inc rabbit anti-mouse alpha smooth muscle actin (a-sma
    Figure 3. Cep induced liver damage. A, Serum levels of AST and ALT in Apoe−/− and Ldlr−/− mice treated with or without Cep. n = 9 for each group in Apoe−/− mice; n = 8 for the Veh group and n = 6 for the Cep group in Ldlr−/− mice; B, Gross images of liver from Apoe−/− and Ldlr−/− mice treated with or without Cep. n = 6 for the Veh group and n = 7 for the Cep group in Apoe−/− mice; n = 8 for the Veh group and n = 6 for the Cep group in Ldlr−/− mice. Scale bar: 1 cm; C, Liver weight and liver weight index in Apoe−/− and Ldlr−/− mice treated with or without Cep; D, H&E staining of livers from Apoe−/− and Ldlr−/− mice treated with or without Cep. Both internal and peripheral liver sections were captured. n = 9 for the Veh group and n = 8 for the Cep group in Apoe−/− mice; n = 7 for the Veh group and n = 6 for the Cep group in Ldlr−/− mice. Scale bar: 20 μm; E, Sirius red staining of liver sections from Apoe−/− and Ldlr−/− mice treated with or without Cep. Internal and peripheral liver sections were captured. Scale bar: 50 μm; F, Immunofluorescence staining of COL1A1 in liver sections from Apoe−/− and Ldlr−/− mice. Scale bar: 50 μm. n = 5 for each group; G, Immunofluorescence staining <t>of</t> <t>α-SMA</t> in liver sections from Apoe−/− and Ldlr−/− mice liver. Scale bar: 100 μm. n = 5 for each group. All data are presented as the means ± SD. Data for ALT in Apoe−/− mice, and AST and ALT in Ldlr−/− mice were analyzed using the Kolmogorov- Smirnov test. Data for AST in Apoe−/− mice were analyzed using an unpaired Student t test. For C, liver weight in Apoe−/− mice was analyzed using the Kolmogorov-Smirnov test; liver weight index in Apoe−/− mice, and liver weight and liver weight index in Ldlr−/− mice were analyzed using an unpaired Student t test. ALT: alanine aminotransferase; AST: aspartate aminotransferase; Cep: cepharanthine; COL1A1: collagen type I alpha 1; DAPI: 4’-6-diamidino-2- phenylindole; H&E: hematoxylin and eosin; SD: standard <t>deviation;</t> <t>α-SMA:</t> alpha-smooth muscle actin; Veh: vehicle.
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    Figure 3. Cep induced liver damage. A, Serum levels of AST and ALT in Apoe−/− and Ldlr−/− mice treated with or without Cep. n = 9 for each group in Apoe−/− mice; n = 8 for the Veh group and n = 6 for the Cep group in Ldlr−/− mice; B, Gross images of liver from Apoe−/− and Ldlr−/− mice treated with or without Cep. n = 6 for the Veh group and n = 7 for the Cep group in Apoe−/− mice; n = 8 for the Veh group and n = 6 for the Cep group in Ldlr−/− mice. Scale bar: 1 cm; C, Liver weight and liver weight index in Apoe−/− and Ldlr−/− mice treated with or without Cep; D, H&E staining of livers from Apoe−/− and Ldlr−/− mice treated with or without Cep. Both internal and peripheral liver sections were captured. n = 9 for the Veh group and n = 8 for the Cep group in Apoe−/− mice; n = 7 for the Veh group and n = 6 for the Cep group in Ldlr−/− mice. Scale bar: 20 μm; E, Sirius red staining of liver sections from Apoe−/− and Ldlr−/− mice treated with or without Cep. Internal and peripheral liver sections were captured. Scale bar: 50 μm; F, Immunofluorescence staining of COL1A1 in liver sections from Apoe−/− and Ldlr−/− mice. Scale bar: 50 μm. n = 5 for each group; G, Immunofluorescence staining of α-SMA in liver sections from Apoe−/− and Ldlr−/− mice liver. Scale bar: 100 μm. n = 5 for each group. All data are presented as the means ± SD. Data for ALT in Apoe−/− mice, and AST and ALT in Ldlr−/− mice were analyzed using the Kolmogorov- Smirnov test. Data for AST in Apoe−/− mice were analyzed using an unpaired Student t test. For C, liver weight in Apoe−/− mice was analyzed using the Kolmogorov-Smirnov test; liver weight index in Apoe−/− mice, and liver weight and liver weight index in Ldlr−/− mice were analyzed using an unpaired Student t test. ALT: alanine aminotransferase; AST: aspartate aminotransferase; Cep: cepharanthine; COL1A1: collagen type I alpha 1; DAPI: 4’-6-diamidino-2- phenylindole; H&E: hematoxylin and eosin; SD: standard deviation; α-SMA: alpha-smooth muscle actin; Veh: vehicle.

    Journal: Cardiology Plus

    Article Title: Cepharanthine aggravated atherosclerosis and liver injury in Apoe −/− and Ldlr −/− mice

    doi: 10.1097/cp9.0000000000000109

    Figure Lengend Snippet: Figure 3. Cep induced liver damage. A, Serum levels of AST and ALT in Apoe−/− and Ldlr−/− mice treated with or without Cep. n = 9 for each group in Apoe−/− mice; n = 8 for the Veh group and n = 6 for the Cep group in Ldlr−/− mice; B, Gross images of liver from Apoe−/− and Ldlr−/− mice treated with or without Cep. n = 6 for the Veh group and n = 7 for the Cep group in Apoe−/− mice; n = 8 for the Veh group and n = 6 for the Cep group in Ldlr−/− mice. Scale bar: 1 cm; C, Liver weight and liver weight index in Apoe−/− and Ldlr−/− mice treated with or without Cep; D, H&E staining of livers from Apoe−/− and Ldlr−/− mice treated with or without Cep. Both internal and peripheral liver sections were captured. n = 9 for the Veh group and n = 8 for the Cep group in Apoe−/− mice; n = 7 for the Veh group and n = 6 for the Cep group in Ldlr−/− mice. Scale bar: 20 μm; E, Sirius red staining of liver sections from Apoe−/− and Ldlr−/− mice treated with or without Cep. Internal and peripheral liver sections were captured. Scale bar: 50 μm; F, Immunofluorescence staining of COL1A1 in liver sections from Apoe−/− and Ldlr−/− mice. Scale bar: 50 μm. n = 5 for each group; G, Immunofluorescence staining of α-SMA in liver sections from Apoe−/− and Ldlr−/− mice liver. Scale bar: 100 μm. n = 5 for each group. All data are presented as the means ± SD. Data for ALT in Apoe−/− mice, and AST and ALT in Ldlr−/− mice were analyzed using the Kolmogorov- Smirnov test. Data for AST in Apoe−/− mice were analyzed using an unpaired Student t test. For C, liver weight in Apoe−/− mice was analyzed using the Kolmogorov-Smirnov test; liver weight index in Apoe−/− mice, and liver weight and liver weight index in Ldlr−/− mice were analyzed using an unpaired Student t test. ALT: alanine aminotransferase; AST: aspartate aminotransferase; Cep: cepharanthine; COL1A1: collagen type I alpha 1; DAPI: 4’-6-diamidino-2- phenylindole; H&E: hematoxylin and eosin; SD: standard deviation; α-SMA: alpha-smooth muscle actin; Veh: vehicle.

    Article Snippet: Primary antibodies include rabbit anti-mouse α-SMA antibody (14395-1-AP; Proteintech, Rosemont, Illinois, USA) and collagen type I monoclonal antibody (67288-1- Ig; Proteintech), both diluted at 1:500.

    Techniques: Staining, Immunofluorescence, Standard Deviation