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Dojindo Labs cygb
Effect of <t>Cygb</t> deficiency in the expression of bile transporters and CD10 in acute <t>BDL</t> mice. Hepatic mRNA level of ( A ) sinusoidal (Mrp2, Mdr2, Bsep) and ( B ) canalicular (Mrp3, Ntcp, Oatp1) transporters of bile components in sham (S) and acute BDL (24–48 h) mice. ( C ) Immunofluorescence (top panels) and immunoblot (bottom panels) of CD10 in sham and BDL-24 h mice. GAPDH was used as loading control. All gels were run under the same experimental conditions. The cropped gels are used and full-length gels are presented in Supplementary Fig. S9 . ( D ) Quantitative densitometry of CD10 (top panel) and hepatic mRNA level (bottom panel) of CD10 in sham (S) and acute BDL (24–72 h) and chronic BDL (1–3 W) mice. Open bars, WT; close bars, Cygb −/− . Data represent the mean ± SD. Sham (n = 3), BDL (n = 4–8). *p
Cygb, supplied by Dojindo Labs, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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1) Product Images from "Possible Involvement of Nitric Oxide in Enhanced Liver Injury and Fibrogenesis during Cholestasis in Cytoglobin-deficient Mice"

Article Title: Possible Involvement of Nitric Oxide in Enhanced Liver Injury and Fibrogenesis during Cholestasis in Cytoglobin-deficient Mice

Journal: Scientific Reports

doi: 10.1038/srep41888

Effect of Cygb deficiency in the expression of bile transporters and CD10 in acute BDL mice. Hepatic mRNA level of ( A ) sinusoidal (Mrp2, Mdr2, Bsep) and ( B ) canalicular (Mrp3, Ntcp, Oatp1) transporters of bile components in sham (S) and acute BDL (24–48 h) mice. ( C ) Immunofluorescence (top panels) and immunoblot (bottom panels) of CD10 in sham and BDL-24 h mice. GAPDH was used as loading control. All gels were run under the same experimental conditions. The cropped gels are used and full-length gels are presented in Supplementary Fig. S9 . ( D ) Quantitative densitometry of CD10 (top panel) and hepatic mRNA level (bottom panel) of CD10 in sham (S) and acute BDL (24–72 h) and chronic BDL (1–3 W) mice. Open bars, WT; close bars, Cygb −/− . Data represent the mean ± SD. Sham (n = 3), BDL (n = 4–8). *p
Figure Legend Snippet: Effect of Cygb deficiency in the expression of bile transporters and CD10 in acute BDL mice. Hepatic mRNA level of ( A ) sinusoidal (Mrp2, Mdr2, Bsep) and ( B ) canalicular (Mrp3, Ntcp, Oatp1) transporters of bile components in sham (S) and acute BDL (24–48 h) mice. ( C ) Immunofluorescence (top panels) and immunoblot (bottom panels) of CD10 in sham and BDL-24 h mice. GAPDH was used as loading control. All gels were run under the same experimental conditions. The cropped gels are used and full-length gels are presented in Supplementary Fig. S9 . ( D ) Quantitative densitometry of CD10 (top panel) and hepatic mRNA level (bottom panel) of CD10 in sham (S) and acute BDL (24–72 h) and chronic BDL (1–3 W) mice. Open bars, WT; close bars, Cygb −/− . Data represent the mean ± SD. Sham (n = 3), BDL (n = 4–8). *p

Techniques Used: Expressing, Mouse Assay, Immunofluorescence

Effect of Cygb deficiency on inflammation and cell death in acute BDL. ( A ) Hepatic mRNA level of chemokine Cxcl-1, Cxcl-2, Cxcl-5, and Ccl-2 in sham (S) and acute BDL (24–48 h). ( B ) Immunohistochemistry of neutrophil- (top panels) and CD68- positive cells (bottom panels) in sham and BDL-24 h mice. ( C ) Quantification of neutrophil- (top panel) and CD68-positive cells (bottom panel) per field. ( D ) TUNEL staining in sham and acute BDL-24 (top panels) and number of TUNEL positive cells (bottom panel) per field. ( E ) Immunoblots of phosphorylated (p) and total NF-κB p65, active and pro caspase 3 (CASP 3), and cytochrome c (CYT C) in sham and BDL-24 h mice. GAPDH was used as loading control. All gels were run under the same experimental conditions. The cropped gels are used and full-length gels are presented in Supplementary Fig. S8 . ( E ) Quantitative densitometry of p-NF-κB and active CASP 3 in sham and BDL-24 h. Open bars, WT; close bars, Cygb −/− . Data represent the mean ± SD. Sham (n = 3), BDL (n = 4–8). *p
Figure Legend Snippet: Effect of Cygb deficiency on inflammation and cell death in acute BDL. ( A ) Hepatic mRNA level of chemokine Cxcl-1, Cxcl-2, Cxcl-5, and Ccl-2 in sham (S) and acute BDL (24–48 h). ( B ) Immunohistochemistry of neutrophil- (top panels) and CD68- positive cells (bottom panels) in sham and BDL-24 h mice. ( C ) Quantification of neutrophil- (top panel) and CD68-positive cells (bottom panel) per field. ( D ) TUNEL staining in sham and acute BDL-24 (top panels) and number of TUNEL positive cells (bottom panel) per field. ( E ) Immunoblots of phosphorylated (p) and total NF-κB p65, active and pro caspase 3 (CASP 3), and cytochrome c (CYT C) in sham and BDL-24 h mice. GAPDH was used as loading control. All gels were run under the same experimental conditions. The cropped gels are used and full-length gels are presented in Supplementary Fig. S8 . ( E ) Quantitative densitometry of p-NF-κB and active CASP 3 in sham and BDL-24 h. Open bars, WT; close bars, Cygb −/− . Data represent the mean ± SD. Sham (n = 3), BDL (n = 4–8). *p

Techniques Used: Immunohistochemistry, Mouse Assay, TUNEL Assay, Staining, Western Blot

Effect of NO inhibitor in Cygb −/− mice after BDL. WT and KO mice were subjected to BDL-48 h together with L-NG-nitroarginine methyl ester (L-NAME) treatment. Control mice received drinking water (DW). ( A ) Concentration of nitrite + nitrate and cGMP in serum. ( B ) Representative macroscopic images and microscopic liver sections stained with H E. ( C ) Serum levels of AST, ALT, total bilirubin, and total bile acid (TBA). ( D ) Immunofluorescence, immunoblots and hepatic mRNA level of CD10. GAPDH was used as loading control. All gels were run under the same experimental conditions. The cropped gels are used and full-length gels are presented in Supplementary Fig. S11 . ( E ) Hepatic mRNA level of Bsep, Mdr2, Oatp1, Ntcp. ( F ) Immunohistochemistry of neutrophils and CD68 and its quantitative analyses (right insets). Open bars, WT; close bars, KO. Data represent the mean ± SD. n = 5. *p
Figure Legend Snippet: Effect of NO inhibitor in Cygb −/− mice after BDL. WT and KO mice were subjected to BDL-48 h together with L-NG-nitroarginine methyl ester (L-NAME) treatment. Control mice received drinking water (DW). ( A ) Concentration of nitrite + nitrate and cGMP in serum. ( B ) Representative macroscopic images and microscopic liver sections stained with H E. ( C ) Serum levels of AST, ALT, total bilirubin, and total bile acid (TBA). ( D ) Immunofluorescence, immunoblots and hepatic mRNA level of CD10. GAPDH was used as loading control. All gels were run under the same experimental conditions. The cropped gels are used and full-length gels are presented in Supplementary Fig. S11 . ( E ) Hepatic mRNA level of Bsep, Mdr2, Oatp1, Ntcp. ( F ) Immunohistochemistry of neutrophils and CD68 and its quantitative analyses (right insets). Open bars, WT; close bars, KO. Data represent the mean ± SD. n = 5. *p

Techniques Used: Mouse Assay, Concentration Assay, Staining, AST Assay, Immunofluorescence, Western Blot, Immunohistochemistry

NO metabolites and oxidative stress condition in Cygb −/− mice under acute BDL. Concentration of nitrite + nitrate ( A ) and cGMP ( B ) in serum, liver lysate and urine in sham (S) and acute BDL-48 h mice. ( C ) Hepatic immunofluorescence, immunoblot and mRNA level of iNOS in sham and acute BDL (24–48 h) mice. ( D ) Malondialdehyde (MDA) content of sham (S) and acute BDL (24–48 h) mice in serum and liver. ( E ) Hepatic immunofluorescence, immunoblot and mRNA of HO-1 in sham or acute BDL mice (24–48 h). GAPDH was used as loading control. All gels were run under the same experimental conditions. The cropped gels are used and full-length gels are presented in Supplementary Fig. S10 . Open bars, WT; close bars, Cygb −/− . Data represent the mean ± SD. Sham (n = 3), BDL (n = 4–8). *p
Figure Legend Snippet: NO metabolites and oxidative stress condition in Cygb −/− mice under acute BDL. Concentration of nitrite + nitrate ( A ) and cGMP ( B ) in serum, liver lysate and urine in sham (S) and acute BDL-48 h mice. ( C ) Hepatic immunofluorescence, immunoblot and mRNA level of iNOS in sham and acute BDL (24–48 h) mice. ( D ) Malondialdehyde (MDA) content of sham (S) and acute BDL (24–48 h) mice in serum and liver. ( E ) Hepatic immunofluorescence, immunoblot and mRNA of HO-1 in sham or acute BDL mice (24–48 h). GAPDH was used as loading control. All gels were run under the same experimental conditions. The cropped gels are used and full-length gels are presented in Supplementary Fig. S10 . Open bars, WT; close bars, Cygb −/− . Data represent the mean ± SD. Sham (n = 3), BDL (n = 4–8). *p

Techniques Used: Mouse Assay, Concentration Assay, Immunofluorescence, Multiple Displacement Amplification

Effect of NO donor on BDL-induced liver injury in WT and Cygb −/− mice after BDL. WT and KO were subjected to BDL-48 h together with saline or sodium nitroprusside (SNP) treatment. ( A ) Concentration of nitrite + nitrate and cGMP in serum. ( B ) Representative macroscopic images, microscopic liver sections stained with H E. ( C ) Serum AST, ALT, total bilirubin, and total bile acid (TBA). ( D ) Immunofluorescent staining, immunoblots and hepatic mRNA level of CD10. GAPDH was used as loading control. All gels were run under the same experimental conditions. The cropped gels are used and full-length gels are presented in Supplementary Fig. S12 . ( E ) Hepatic mRNA level of Bsep, Mdr2, Oatp1, Ntcp. ( F ) Immunohistochemistry of neutrophils and CD68 and its quantitative analyses (right insets). Open bars, WT; close bars, KO. Data represent the mean ± SD. n = 5. *p
Figure Legend Snippet: Effect of NO donor on BDL-induced liver injury in WT and Cygb −/− mice after BDL. WT and KO were subjected to BDL-48 h together with saline or sodium nitroprusside (SNP) treatment. ( A ) Concentration of nitrite + nitrate and cGMP in serum. ( B ) Representative macroscopic images, microscopic liver sections stained with H E. ( C ) Serum AST, ALT, total bilirubin, and total bile acid (TBA). ( D ) Immunofluorescent staining, immunoblots and hepatic mRNA level of CD10. GAPDH was used as loading control. All gels were run under the same experimental conditions. The cropped gels are used and full-length gels are presented in Supplementary Fig. S12 . ( E ) Hepatic mRNA level of Bsep, Mdr2, Oatp1, Ntcp. ( F ) Immunohistochemistry of neutrophils and CD68 and its quantitative analyses (right insets). Open bars, WT; close bars, KO. Data represent the mean ± SD. n = 5. *p

Techniques Used: Mouse Assay, Concentration Assay, Staining, AST Assay, Western Blot, Immunohistochemistry

Severe liver injury in Cygb −/− mice under BDL. ( A ) Kaplan-Meier curve, n = 19 per group. Representative macroscopic images ( B ) and microscopic liver sections stained with H E ( C ) in sham, acute BDL (24–72 h) and chronic BDL (1–3 W). Original magnification, x40. Yellow and black arrows indicate bile infarcts. ( D ) Quantification of area of bile infarcts. ( E ) Levels of serum AST, ALT, and total bilirubin, and hepatic total bile acid (TBA). Data represent the mean ± SD. Sham (n = 3), BDL (n = 4–8). *p
Figure Legend Snippet: Severe liver injury in Cygb −/− mice under BDL. ( A ) Kaplan-Meier curve, n = 19 per group. Representative macroscopic images ( B ) and microscopic liver sections stained with H E ( C ) in sham, acute BDL (24–72 h) and chronic BDL (1–3 W). Original magnification, x40. Yellow and black arrows indicate bile infarcts. ( D ) Quantification of area of bile infarcts. ( E ) Levels of serum AST, ALT, and total bilirubin, and hepatic total bile acid (TBA). Data represent the mean ± SD. Sham (n = 3), BDL (n = 4–8). *p

Techniques Used: Mouse Assay, Staining, AST Assay

Promotion of fibrosis in Cygb −/− mice after chronic BDL. ( A ) Liver sections from Sirius Red and Fast Green (SiR-FG) staining in BDL 2 W. ( B ) Sirius Red positive area (left panel) and hydroxyproline (HP) content of liver (right panel) in sham (S) and chronic BDL (1–3 W) mice. ( C ) Immunohistochemistry for α-SMA (top panels), immunoblot analysis (bottom panels), and its quantitative densitometry (right inset) of the α-SMA expression. GAPDH was used as loading control. All gels were run under the same experimental conditions. The cropped gels are used and full-length gels are presented in Supplementary Fig. S13 . ( D ) Hepatic mRNA level of α-Sma expression. ( E ) Hepatic mRNA level of collagen1a1 and Timp-1. Open bars, WT; close bars, KO. Data represent the mean ± SD. Sham (n = 3), BDL (n = 4–8). *p
Figure Legend Snippet: Promotion of fibrosis in Cygb −/− mice after chronic BDL. ( A ) Liver sections from Sirius Red and Fast Green (SiR-FG) staining in BDL 2 W. ( B ) Sirius Red positive area (left panel) and hydroxyproline (HP) content of liver (right panel) in sham (S) and chronic BDL (1–3 W) mice. ( C ) Immunohistochemistry for α-SMA (top panels), immunoblot analysis (bottom panels), and its quantitative densitometry (right inset) of the α-SMA expression. GAPDH was used as loading control. All gels were run under the same experimental conditions. The cropped gels are used and full-length gels are presented in Supplementary Fig. S13 . ( D ) Hepatic mRNA level of α-Sma expression. ( E ) Hepatic mRNA level of collagen1a1 and Timp-1. Open bars, WT; close bars, KO. Data represent the mean ± SD. Sham (n = 3), BDL (n = 4–8). *p

Techniques Used: Mouse Assay, Staining, Immunohistochemistry, Expressing

Related Articles

Mouse Assay:

Article Title: Possible Involvement of Nitric Oxide in Enhanced Liver Injury and Fibrogenesis during Cholestasis in Cytoglobin-deficient Mice
Article Snippet: .. Treatment of nitric oxide inhibitor and donor To investigate the role of NO in BDL model, WT or Cygb−/− mice were administered L-NAME (Dojindo, MD, USA) in drinking water at the dose of 0.5 mg/ml for 9 days (n = 5 per each group). .. In NO donor treatment, WT or Cygb−/− mice were received 3 doses of SNP (2 mg/kg body weight) (Millipore Corp., Billerica, MA, USA) or saline by i.p. injection (n = 5 per each group).

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    Dojindo Labs cygb
    Effect of <t>Cygb</t> deficiency in the expression of bile transporters and CD10 in acute <t>BDL</t> mice. Hepatic mRNA level of ( A ) sinusoidal (Mrp2, Mdr2, Bsep) and ( B ) canalicular (Mrp3, Ntcp, Oatp1) transporters of bile components in sham (S) and acute BDL (24–48 h) mice. ( C ) Immunofluorescence (top panels) and immunoblot (bottom panels) of CD10 in sham and BDL-24 h mice. GAPDH was used as loading control. All gels were run under the same experimental conditions. The cropped gels are used and full-length gels are presented in Supplementary Fig. S9 . ( D ) Quantitative densitometry of CD10 (top panel) and hepatic mRNA level (bottom panel) of CD10 in sham (S) and acute BDL (24–72 h) and chronic BDL (1–3 W) mice. Open bars, WT; close bars, Cygb −/− . Data represent the mean ± SD. Sham (n = 3), BDL (n = 4–8). *p
    Cygb, supplied by Dojindo Labs, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/cygb/product/Dojindo Labs
    Average 91 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    cygb - by Bioz Stars, 2020-08
    91/100 stars
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    Effect of Cygb deficiency in the expression of bile transporters and CD10 in acute BDL mice. Hepatic mRNA level of ( A ) sinusoidal (Mrp2, Mdr2, Bsep) and ( B ) canalicular (Mrp3, Ntcp, Oatp1) transporters of bile components in sham (S) and acute BDL (24–48 h) mice. ( C ) Immunofluorescence (top panels) and immunoblot (bottom panels) of CD10 in sham and BDL-24 h mice. GAPDH was used as loading control. All gels were run under the same experimental conditions. The cropped gels are used and full-length gels are presented in Supplementary Fig. S9 . ( D ) Quantitative densitometry of CD10 (top panel) and hepatic mRNA level (bottom panel) of CD10 in sham (S) and acute BDL (24–72 h) and chronic BDL (1–3 W) mice. Open bars, WT; close bars, Cygb −/− . Data represent the mean ± SD. Sham (n = 3), BDL (n = 4–8). *p

    Journal: Scientific Reports

    Article Title: Possible Involvement of Nitric Oxide in Enhanced Liver Injury and Fibrogenesis during Cholestasis in Cytoglobin-deficient Mice

    doi: 10.1038/srep41888

    Figure Lengend Snippet: Effect of Cygb deficiency in the expression of bile transporters and CD10 in acute BDL mice. Hepatic mRNA level of ( A ) sinusoidal (Mrp2, Mdr2, Bsep) and ( B ) canalicular (Mrp3, Ntcp, Oatp1) transporters of bile components in sham (S) and acute BDL (24–48 h) mice. ( C ) Immunofluorescence (top panels) and immunoblot (bottom panels) of CD10 in sham and BDL-24 h mice. GAPDH was used as loading control. All gels were run under the same experimental conditions. The cropped gels are used and full-length gels are presented in Supplementary Fig. S9 . ( D ) Quantitative densitometry of CD10 (top panel) and hepatic mRNA level (bottom panel) of CD10 in sham (S) and acute BDL (24–72 h) and chronic BDL (1–3 W) mice. Open bars, WT; close bars, Cygb −/− . Data represent the mean ± SD. Sham (n = 3), BDL (n = 4–8). *p

    Article Snippet: Treatment of nitric oxide inhibitor and donor To investigate the role of NO in BDL model, WT or Cygb−/− mice were administered L-NAME (Dojindo, MD, USA) in drinking water at the dose of 0.5 mg/ml for 9 days (n = 5 per each group).

    Techniques: Expressing, Mouse Assay, Immunofluorescence

    Effect of Cygb deficiency on inflammation and cell death in acute BDL. ( A ) Hepatic mRNA level of chemokine Cxcl-1, Cxcl-2, Cxcl-5, and Ccl-2 in sham (S) and acute BDL (24–48 h). ( B ) Immunohistochemistry of neutrophil- (top panels) and CD68- positive cells (bottom panels) in sham and BDL-24 h mice. ( C ) Quantification of neutrophil- (top panel) and CD68-positive cells (bottom panel) per field. ( D ) TUNEL staining in sham and acute BDL-24 (top panels) and number of TUNEL positive cells (bottom panel) per field. ( E ) Immunoblots of phosphorylated (p) and total NF-κB p65, active and pro caspase 3 (CASP 3), and cytochrome c (CYT C) in sham and BDL-24 h mice. GAPDH was used as loading control. All gels were run under the same experimental conditions. The cropped gels are used and full-length gels are presented in Supplementary Fig. S8 . ( E ) Quantitative densitometry of p-NF-κB and active CASP 3 in sham and BDL-24 h. Open bars, WT; close bars, Cygb −/− . Data represent the mean ± SD. Sham (n = 3), BDL (n = 4–8). *p

    Journal: Scientific Reports

    Article Title: Possible Involvement of Nitric Oxide in Enhanced Liver Injury and Fibrogenesis during Cholestasis in Cytoglobin-deficient Mice

    doi: 10.1038/srep41888

    Figure Lengend Snippet: Effect of Cygb deficiency on inflammation and cell death in acute BDL. ( A ) Hepatic mRNA level of chemokine Cxcl-1, Cxcl-2, Cxcl-5, and Ccl-2 in sham (S) and acute BDL (24–48 h). ( B ) Immunohistochemistry of neutrophil- (top panels) and CD68- positive cells (bottom panels) in sham and BDL-24 h mice. ( C ) Quantification of neutrophil- (top panel) and CD68-positive cells (bottom panel) per field. ( D ) TUNEL staining in sham and acute BDL-24 (top panels) and number of TUNEL positive cells (bottom panel) per field. ( E ) Immunoblots of phosphorylated (p) and total NF-κB p65, active and pro caspase 3 (CASP 3), and cytochrome c (CYT C) in sham and BDL-24 h mice. GAPDH was used as loading control. All gels were run under the same experimental conditions. The cropped gels are used and full-length gels are presented in Supplementary Fig. S8 . ( E ) Quantitative densitometry of p-NF-κB and active CASP 3 in sham and BDL-24 h. Open bars, WT; close bars, Cygb −/− . Data represent the mean ± SD. Sham (n = 3), BDL (n = 4–8). *p

    Article Snippet: Treatment of nitric oxide inhibitor and donor To investigate the role of NO in BDL model, WT or Cygb−/− mice were administered L-NAME (Dojindo, MD, USA) in drinking water at the dose of 0.5 mg/ml for 9 days (n = 5 per each group).

    Techniques: Immunohistochemistry, Mouse Assay, TUNEL Assay, Staining, Western Blot

    Effect of NO inhibitor in Cygb −/− mice after BDL. WT and KO mice were subjected to BDL-48 h together with L-NG-nitroarginine methyl ester (L-NAME) treatment. Control mice received drinking water (DW). ( A ) Concentration of nitrite + nitrate and cGMP in serum. ( B ) Representative macroscopic images and microscopic liver sections stained with H E. ( C ) Serum levels of AST, ALT, total bilirubin, and total bile acid (TBA). ( D ) Immunofluorescence, immunoblots and hepatic mRNA level of CD10. GAPDH was used as loading control. All gels were run under the same experimental conditions. The cropped gels are used and full-length gels are presented in Supplementary Fig. S11 . ( E ) Hepatic mRNA level of Bsep, Mdr2, Oatp1, Ntcp. ( F ) Immunohistochemistry of neutrophils and CD68 and its quantitative analyses (right insets). Open bars, WT; close bars, KO. Data represent the mean ± SD. n = 5. *p

    Journal: Scientific Reports

    Article Title: Possible Involvement of Nitric Oxide in Enhanced Liver Injury and Fibrogenesis during Cholestasis in Cytoglobin-deficient Mice

    doi: 10.1038/srep41888

    Figure Lengend Snippet: Effect of NO inhibitor in Cygb −/− mice after BDL. WT and KO mice were subjected to BDL-48 h together with L-NG-nitroarginine methyl ester (L-NAME) treatment. Control mice received drinking water (DW). ( A ) Concentration of nitrite + nitrate and cGMP in serum. ( B ) Representative macroscopic images and microscopic liver sections stained with H E. ( C ) Serum levels of AST, ALT, total bilirubin, and total bile acid (TBA). ( D ) Immunofluorescence, immunoblots and hepatic mRNA level of CD10. GAPDH was used as loading control. All gels were run under the same experimental conditions. The cropped gels are used and full-length gels are presented in Supplementary Fig. S11 . ( E ) Hepatic mRNA level of Bsep, Mdr2, Oatp1, Ntcp. ( F ) Immunohistochemistry of neutrophils and CD68 and its quantitative analyses (right insets). Open bars, WT; close bars, KO. Data represent the mean ± SD. n = 5. *p

    Article Snippet: Treatment of nitric oxide inhibitor and donor To investigate the role of NO in BDL model, WT or Cygb−/− mice were administered L-NAME (Dojindo, MD, USA) in drinking water at the dose of 0.5 mg/ml for 9 days (n = 5 per each group).

    Techniques: Mouse Assay, Concentration Assay, Staining, AST Assay, Immunofluorescence, Western Blot, Immunohistochemistry

    NO metabolites and oxidative stress condition in Cygb −/− mice under acute BDL. Concentration of nitrite + nitrate ( A ) and cGMP ( B ) in serum, liver lysate and urine in sham (S) and acute BDL-48 h mice. ( C ) Hepatic immunofluorescence, immunoblot and mRNA level of iNOS in sham and acute BDL (24–48 h) mice. ( D ) Malondialdehyde (MDA) content of sham (S) and acute BDL (24–48 h) mice in serum and liver. ( E ) Hepatic immunofluorescence, immunoblot and mRNA of HO-1 in sham or acute BDL mice (24–48 h). GAPDH was used as loading control. All gels were run under the same experimental conditions. The cropped gels are used and full-length gels are presented in Supplementary Fig. S10 . Open bars, WT; close bars, Cygb −/− . Data represent the mean ± SD. Sham (n = 3), BDL (n = 4–8). *p

    Journal: Scientific Reports

    Article Title: Possible Involvement of Nitric Oxide in Enhanced Liver Injury and Fibrogenesis during Cholestasis in Cytoglobin-deficient Mice

    doi: 10.1038/srep41888

    Figure Lengend Snippet: NO metabolites and oxidative stress condition in Cygb −/− mice under acute BDL. Concentration of nitrite + nitrate ( A ) and cGMP ( B ) in serum, liver lysate and urine in sham (S) and acute BDL-48 h mice. ( C ) Hepatic immunofluorescence, immunoblot and mRNA level of iNOS in sham and acute BDL (24–48 h) mice. ( D ) Malondialdehyde (MDA) content of sham (S) and acute BDL (24–48 h) mice in serum and liver. ( E ) Hepatic immunofluorescence, immunoblot and mRNA of HO-1 in sham or acute BDL mice (24–48 h). GAPDH was used as loading control. All gels were run under the same experimental conditions. The cropped gels are used and full-length gels are presented in Supplementary Fig. S10 . Open bars, WT; close bars, Cygb −/− . Data represent the mean ± SD. Sham (n = 3), BDL (n = 4–8). *p

    Article Snippet: Treatment of nitric oxide inhibitor and donor To investigate the role of NO in BDL model, WT or Cygb−/− mice were administered L-NAME (Dojindo, MD, USA) in drinking water at the dose of 0.5 mg/ml for 9 days (n = 5 per each group).

    Techniques: Mouse Assay, Concentration Assay, Immunofluorescence, Multiple Displacement Amplification

    Effect of NO donor on BDL-induced liver injury in WT and Cygb −/− mice after BDL. WT and KO were subjected to BDL-48 h together with saline or sodium nitroprusside (SNP) treatment. ( A ) Concentration of nitrite + nitrate and cGMP in serum. ( B ) Representative macroscopic images, microscopic liver sections stained with H E. ( C ) Serum AST, ALT, total bilirubin, and total bile acid (TBA). ( D ) Immunofluorescent staining, immunoblots and hepatic mRNA level of CD10. GAPDH was used as loading control. All gels were run under the same experimental conditions. The cropped gels are used and full-length gels are presented in Supplementary Fig. S12 . ( E ) Hepatic mRNA level of Bsep, Mdr2, Oatp1, Ntcp. ( F ) Immunohistochemistry of neutrophils and CD68 and its quantitative analyses (right insets). Open bars, WT; close bars, KO. Data represent the mean ± SD. n = 5. *p

    Journal: Scientific Reports

    Article Title: Possible Involvement of Nitric Oxide in Enhanced Liver Injury and Fibrogenesis during Cholestasis in Cytoglobin-deficient Mice

    doi: 10.1038/srep41888

    Figure Lengend Snippet: Effect of NO donor on BDL-induced liver injury in WT and Cygb −/− mice after BDL. WT and KO were subjected to BDL-48 h together with saline or sodium nitroprusside (SNP) treatment. ( A ) Concentration of nitrite + nitrate and cGMP in serum. ( B ) Representative macroscopic images, microscopic liver sections stained with H E. ( C ) Serum AST, ALT, total bilirubin, and total bile acid (TBA). ( D ) Immunofluorescent staining, immunoblots and hepatic mRNA level of CD10. GAPDH was used as loading control. All gels were run under the same experimental conditions. The cropped gels are used and full-length gels are presented in Supplementary Fig. S12 . ( E ) Hepatic mRNA level of Bsep, Mdr2, Oatp1, Ntcp. ( F ) Immunohistochemistry of neutrophils and CD68 and its quantitative analyses (right insets). Open bars, WT; close bars, KO. Data represent the mean ± SD. n = 5. *p

    Article Snippet: Treatment of nitric oxide inhibitor and donor To investigate the role of NO in BDL model, WT or Cygb−/− mice were administered L-NAME (Dojindo, MD, USA) in drinking water at the dose of 0.5 mg/ml for 9 days (n = 5 per each group).

    Techniques: Mouse Assay, Concentration Assay, Staining, AST Assay, Western Blot, Immunohistochemistry

    Severe liver injury in Cygb −/− mice under BDL. ( A ) Kaplan-Meier curve, n = 19 per group. Representative macroscopic images ( B ) and microscopic liver sections stained with H E ( C ) in sham, acute BDL (24–72 h) and chronic BDL (1–3 W). Original magnification, x40. Yellow and black arrows indicate bile infarcts. ( D ) Quantification of area of bile infarcts. ( E ) Levels of serum AST, ALT, and total bilirubin, and hepatic total bile acid (TBA). Data represent the mean ± SD. Sham (n = 3), BDL (n = 4–8). *p

    Journal: Scientific Reports

    Article Title: Possible Involvement of Nitric Oxide in Enhanced Liver Injury and Fibrogenesis during Cholestasis in Cytoglobin-deficient Mice

    doi: 10.1038/srep41888

    Figure Lengend Snippet: Severe liver injury in Cygb −/− mice under BDL. ( A ) Kaplan-Meier curve, n = 19 per group. Representative macroscopic images ( B ) and microscopic liver sections stained with H E ( C ) in sham, acute BDL (24–72 h) and chronic BDL (1–3 W). Original magnification, x40. Yellow and black arrows indicate bile infarcts. ( D ) Quantification of area of bile infarcts. ( E ) Levels of serum AST, ALT, and total bilirubin, and hepatic total bile acid (TBA). Data represent the mean ± SD. Sham (n = 3), BDL (n = 4–8). *p

    Article Snippet: Treatment of nitric oxide inhibitor and donor To investigate the role of NO in BDL model, WT or Cygb−/− mice were administered L-NAME (Dojindo, MD, USA) in drinking water at the dose of 0.5 mg/ml for 9 days (n = 5 per each group).

    Techniques: Mouse Assay, Staining, AST Assay

    Promotion of fibrosis in Cygb −/− mice after chronic BDL. ( A ) Liver sections from Sirius Red and Fast Green (SiR-FG) staining in BDL 2 W. ( B ) Sirius Red positive area (left panel) and hydroxyproline (HP) content of liver (right panel) in sham (S) and chronic BDL (1–3 W) mice. ( C ) Immunohistochemistry for α-SMA (top panels), immunoblot analysis (bottom panels), and its quantitative densitometry (right inset) of the α-SMA expression. GAPDH was used as loading control. All gels were run under the same experimental conditions. The cropped gels are used and full-length gels are presented in Supplementary Fig. S13 . ( D ) Hepatic mRNA level of α-Sma expression. ( E ) Hepatic mRNA level of collagen1a1 and Timp-1. Open bars, WT; close bars, KO. Data represent the mean ± SD. Sham (n = 3), BDL (n = 4–8). *p

    Journal: Scientific Reports

    Article Title: Possible Involvement of Nitric Oxide in Enhanced Liver Injury and Fibrogenesis during Cholestasis in Cytoglobin-deficient Mice

    doi: 10.1038/srep41888

    Figure Lengend Snippet: Promotion of fibrosis in Cygb −/− mice after chronic BDL. ( A ) Liver sections from Sirius Red and Fast Green (SiR-FG) staining in BDL 2 W. ( B ) Sirius Red positive area (left panel) and hydroxyproline (HP) content of liver (right panel) in sham (S) and chronic BDL (1–3 W) mice. ( C ) Immunohistochemistry for α-SMA (top panels), immunoblot analysis (bottom panels), and its quantitative densitometry (right inset) of the α-SMA expression. GAPDH was used as loading control. All gels were run under the same experimental conditions. The cropped gels are used and full-length gels are presented in Supplementary Fig. S13 . ( D ) Hepatic mRNA level of α-Sma expression. ( E ) Hepatic mRNA level of collagen1a1 and Timp-1. Open bars, WT; close bars, KO. Data represent the mean ± SD. Sham (n = 3), BDL (n = 4–8). *p

    Article Snippet: Treatment of nitric oxide inhibitor and donor To investigate the role of NO in BDL model, WT or Cygb−/− mice were administered L-NAME (Dojindo, MD, USA) in drinking water at the dose of 0.5 mg/ml for 9 days (n = 5 per each group).

    Techniques: Mouse Assay, Staining, Immunohistochemistry, Expressing