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mcd rifaximin group (MedChemExpress)

Name: mcd rifaximin group
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MedChemExpress mcd rifaximin group

<t>Rifaximin</t> ameliorates non-alcoholic steatohepatitis in <t>MCD</t> diet-fed mice. (A) Photographs of livers in the MCS, MCD and MCD + rifaximin groups. (B) Liver weight, and liver weight to body weight ratio in each group. (C) Haematoxylin and eosin staining of livers in the MCS, MCD and MCD + rifaximin groups. Scale bars, 100 µm. (D) Steatosis score, hepatic ballooning score, interlobular inflammation score and NAS. (E) Oil red O staining of livers in the MCS, MCD and MCD + rifaximin groups. Scale bars, 100 µm. (F) Srebp1, Pparγ and CD36 mRNA expression levels in mouse livers. (G) Plasma ALT and AST levels in mice. n=8 mice/group. *P<0.05, **P<0.01, ***P<0.001, ****P<0.0001. ALT, alanine transaminase; AST, aspartate transaminase; MCD, methionine-choline deficient; MCS, methionine-choline sufficient; NAS, non-alcoholic fatty liver disease activity score; Srebp1, sterol regulatory element-binding protein 1.

Mcd Rifaximin Group, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 93/100, based on 4 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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1) Product Images from "Study on the molecular mechanisms of rifaximin in the treatment of non‑alcoholic steatohepatitis based on the Helicobacter ‑DCA‑Fxr‑Hnf1α signalling pathway"

Article Title: Study on the molecular mechanisms of rifaximin in the treatment of non‑alcoholic steatohepatitis based on the Helicobacter ‑DCA‑Fxr‑Hnf1α signalling pathway

Journal: Molecular Medicine Reports

doi: 10.3892/mmr.2024.13407

Rifaximin ameliorates non-alcoholic steatohepatitis in MCD diet-fed mice. (A) Photographs of livers in the MCS, MCD and MCD + rifaximin groups. (B) Liver weight, and liver weight to body weight ratio in each group. (C) Haematoxylin and eosin staining of livers in the MCS, MCD and MCD + rifaximin groups. Scale bars, 100 µm. (D) Steatosis score, hepatic ballooning score, interlobular inflammation score and NAS. (E) Oil red O staining of livers in the MCS, MCD and MCD + rifaximin groups. Scale bars, 100 µm. (F) Srebp1, Pparγ and CD36 mRNA expression levels in mouse livers. (G) Plasma ALT and AST levels in mice. n=8 mice/group. *P<0.05, **P<0.01, ***P<0.001, ****P<0.0001. ALT, alanine transaminase; AST, aspartate transaminase; MCD, methionine-choline deficient; MCS, methionine-choline sufficient; NAS, non-alcoholic fatty liver disease activity score; Srebp1, sterol regulatory element-binding protein 1.

Figure Legend Snippet: Rifaximin ameliorates non-alcoholic steatohepatitis in MCD diet-fed mice. (A) Photographs of livers in the MCS, MCD and MCD + rifaximin groups. (B) Liver weight, and liver weight to body weight ratio in each group. (C) Haematoxylin and eosin staining of livers in the MCS, MCD and MCD + rifaximin groups. Scale bars, 100 µm. (D) Steatosis score, hepatic ballooning score, interlobular inflammation score and NAS. (E) Oil red O staining of livers in the MCS, MCD and MCD + rifaximin groups. Scale bars, 100 µm. (F) Srebp1, Pparγ and CD36 mRNA expression levels in mouse livers. (G) Plasma ALT and AST levels in mice. n=8 mice/group. *P<0.05, **P<0.01, ***P<0.001, ****P<0.0001. ALT, alanine transaminase; AST, aspartate transaminase; MCD, methionine-choline deficient; MCS, methionine-choline sufficient; NAS, non-alcoholic fatty liver disease activity score; Srebp1, sterol regulatory element-binding protein 1.

Techniques Used: Staining, Expressing, Clinical Proteomics, Activity Assay, Binding Assay

Rifaximin alleviates liver fibrosis in mice with MCD diet-induced non-alcoholic steatohepatitis. (A) Sirius Red staining of livers in each group. Scale bars, 100 µm. (B) α-Sma immunostaining of livers in each group. Scale bars, 100 µm. (C) Col1a1 immunostaining of livers in each group. Scale bars, 100 µm. (D) α-Sma and Col1a1 mRNA expression levels of livers in each group. (E) Hydroxyproline content in mouse livers. n=8 mice/group. *P<0.05, **P<0.01, ***P<0.001. α-Sma, α-smooth muscle actin; Col1a1, collagen type 1 α1; MCD, methionine-choline deficient; MCS, methionine-choline sufficient.

Figure Legend Snippet: Rifaximin alleviates liver fibrosis in mice with MCD diet-induced non-alcoholic steatohepatitis. (A) Sirius Red staining of livers in each group. Scale bars, 100 µm. (B) α-Sma immunostaining of livers in each group. Scale bars, 100 µm. (C) Col1a1 immunostaining of livers in each group. Scale bars, 100 µm. (D) α-Sma and Col1a1 mRNA expression levels of livers in each group. (E) Hydroxyproline content in mouse livers. n=8 mice/group. *P<0.05, **P<0.01, ***P<0.001. α-Sma, α-smooth muscle actin; Col1a1, collagen type 1 α1; MCD, methionine-choline deficient; MCS, methionine-choline sufficient.

Techniques Used: Staining, Immunostaining, Expressing

Rifaximin affects the gut microbiota in mice with MCD diet-induced non-alcoholic steatohepatitis. (A) Caecal OTU, Chao index, Simpson index and Shannon index of mice. (B) Separation of samples by MCS, MCD, and MCD with rifaximin gavage was observed via NMDS analysis. (C) Relative abundance of gut microbiota in caecal content identified by LEfSe bar analysis among MCS, MCD and MCD + rifaximin groups. (D) Heatmap of separation at the phylum level of mouse faecal microbiota among the MCS, MCD and MCD + rifaximin groups. (E) Significant difference in mouse faecal microbiota at the phylum level among the MCS, MCD and MCD + rifaximin groups. (F) Heatmap of separation at the genus level of mouse faecal microflora among the MCS, MCD and MCD + rifaximin groups. (G) Significant difference of mouse faecal microbiota at the genus level among the MCS, MCD and MCD + rifaximin groups. Clustering was performed using the Pearson measurement. *P<0.05, **P<0.01, ***P<0.001. LDA, linear discriminant analysis; MCD, methionine-choline deficient; MCS, methionine-choline sufficient; NMDS, non-metric multidimensional scaling; OTU, operational taxonomic unit.

Figure Legend Snippet: Rifaximin affects the gut microbiota in mice with MCD diet-induced non-alcoholic steatohepatitis. (A) Caecal OTU, Chao index, Simpson index and Shannon index of mice. (B) Separation of samples by MCS, MCD, and MCD with rifaximin gavage was observed via NMDS analysis. (C) Relative abundance of gut microbiota in caecal content identified by LEfSe bar analysis among MCS, MCD and MCD + rifaximin groups. (D) Heatmap of separation at the phylum level of mouse faecal microbiota among the MCS, MCD and MCD + rifaximin groups. (E) Significant difference in mouse faecal microbiota at the phylum level among the MCS, MCD and MCD + rifaximin groups. (F) Heatmap of separation at the genus level of mouse faecal microflora among the MCS, MCD and MCD + rifaximin groups. (G) Significant difference of mouse faecal microbiota at the genus level among the MCS, MCD and MCD + rifaximin groups. Clustering was performed using the Pearson measurement. *P<0.05, **P<0.01, ***P<0.001. LDA, linear discriminant analysis; MCD, methionine-choline deficient; MCS, methionine-choline sufficient; NMDS, non-metric multidimensional scaling; OTU, operational taxonomic unit.

Techniques Used:

Rifaximin suppresses the Helicobacter -DCA-Fxr signalling pathway in MCD diet-fed mice. (A) Correlation analysis of intestinal microflora and BAs in the distal ileum was investigated using nonparametric Spearman's test. (B) BA levels in the distal ileum of mice. (C) Total BAs, conjugated BAs/unconjugated BAs ratio, and primary BAs/second BAs ratio in the distal ileum of mice. (D) Expression levels of Fxr, Fgf15 and Shp in the distal ileum. (E) Expression levels of Cyp7a1, Cyp7b1, Cyp8b1, and Cyp27a1 mRNA in the liver. n=8 mice/group. *P<0.05, **P<0.01, ***P<0.001, ****P<0.0001. BA, bile acid; DCA, deoxycholic acid; Fgf15, fibroblast growth factor 15; Fxr, farnesoid X receptor; MCD, methionine-choline deficient; MCS, methionine-choline sufficient.

Figure Legend Snippet: Rifaximin suppresses the Helicobacter -DCA-Fxr signalling pathway in MCD diet-fed mice. (A) Correlation analysis of intestinal microflora and BAs in the distal ileum was investigated using nonparametric Spearman's test. (B) BA levels in the distal ileum of mice. (C) Total BAs, conjugated BAs/unconjugated BAs ratio, and primary BAs/second BAs ratio in the distal ileum of mice. (D) Expression levels of Fxr, Fgf15 and Shp in the distal ileum. (E) Expression levels of Cyp7a1, Cyp7b1, Cyp8b1, and Cyp27a1 mRNA in the liver. n=8 mice/group. *P<0.05, **P<0.01, ***P<0.001, ****P<0.0001. BA, bile acid; DCA, deoxycholic acid; Fgf15, fibroblast growth factor 15; Fxr, farnesoid X receptor; MCD, methionine-choline deficient; MCS, methionine-choline sufficient.

Techniques Used: Expressing

Anti-NASH effects of rifaximin are impaired in mice lacking gut microbiota. (A) Schematic illustration of the experimental design of intestinal decontamination in mice with NASH. (B) Haematoxylin and eosin staining of livers in the MCD, MCD + rifaximin, MCD + Abx and MCD + Abx + rifaximin groups. Scale bars, 100 µm. (C) Steatosis score, hepatic ballooning score, interlobular inflammation score and NAS. (D) Oil red O staining for livers of mice in each group. Scale bars, 100 µm. (E) Pparγ and Srebp1 protein expression levels in mouse livers. (F) α-Sma protein expression levels in the livers in each group. n=8 mice/group. *P<0.05, **P<0.01, ***P<0.001, ****P<0.0001. α-Sma, α-smooth muscle actin; MCD, methionine-choline deficient; MCS, methionine-choline sufficient; NASH, non-alcoholic steatohepatitis; NAS, non-alcoholic fatty liver disease activity score; Srebp1, sterol regulatory element-binding protein 1.

Figure Legend Snippet: Anti-NASH effects of rifaximin are impaired in mice lacking gut microbiota. (A) Schematic illustration of the experimental design of intestinal decontamination in mice with NASH. (B) Haematoxylin and eosin staining of livers in the MCD, MCD + rifaximin, MCD + Abx and MCD + Abx + rifaximin groups. Scale bars, 100 µm. (C) Steatosis score, hepatic ballooning score, interlobular inflammation score and NAS. (D) Oil red O staining for livers of mice in each group. Scale bars, 100 µm. (E) Pparγ and Srebp1 protein expression levels in mouse livers. (F) α-Sma protein expression levels in the livers in each group. n=8 mice/group. *P<0.05, **P<0.01, ***P<0.001, ****P<0.0001. α-Sma, α-smooth muscle actin; MCD, methionine-choline deficient; MCS, methionine-choline sufficient; NASH, non-alcoholic steatohepatitis; NAS, non-alcoholic fatty liver disease activity score; Srebp1, sterol regulatory element-binding protein 1.

Techniques Used: Staining, Expressing, Activity Assay, Binding Assay

Activation of hepatic Hnf1α is required for rifaximin to ameliorate NASH in mice. (A) Hnf1α H-KO NASH mice were established. (B) Schematic illustration of the experimental design. (C) Hnf1α protein expression levels in the mouse livers of each group. (D) Haematoxylin and eosin staining of livers in each group. Scale bars, 100 µm. (E) Steatosis score, hepatic ballooning score, interlobular inflammation score and NAS. (F) Oil red O staining for livers of mice in each group. Scale bars, 100 µm. (G) Pparγ and Srebp1 protein expression levels in the livers of each group. (H) α-Sma protein expression level in the livers in each group. n=5 mice/group. α-Sma, α-smooth muscle actin; Hnf1α, hepatocyte nuclear factor 1α; Hnf1α f/f , floxed Hnf1α; Hnf1α H-KO , hepatocyte-specific Hnf1α knockout; MCD, methionine-choline deficient; MCS, methionine-choline sufficient; NASH, non-alcoholic steatohepatitis; NAS, non-alcoholic fatty liver disease activity score; Srebp1, sterol regulatory element-binding protein 1.

Figure Legend Snippet: Activation of hepatic Hnf1α is required for rifaximin to ameliorate NASH in mice. (A) Hnf1α H-KO NASH mice were established. (B) Schematic illustration of the experimental design. (C) Hnf1α protein expression levels in the mouse livers of each group. (D) Haematoxylin and eosin staining of livers in each group. Scale bars, 100 µm. (E) Steatosis score, hepatic ballooning score, interlobular inflammation score and NAS. (F) Oil red O staining for livers of mice in each group. Scale bars, 100 µm. (G) Pparγ and Srebp1 protein expression levels in the livers of each group. (H) α-Sma protein expression level in the livers in each group. n=5 mice/group. α-Sma, α-smooth muscle actin; Hnf1α, hepatocyte nuclear factor 1α; Hnf1α f/f , floxed Hnf1α; Hnf1α H-KO , hepatocyte-specific Hnf1α knockout; MCD, methionine-choline deficient; MCS, methionine-choline sufficient; NASH, non-alcoholic steatohepatitis; NAS, non-alcoholic fatty liver disease activity score; Srebp1, sterol regulatory element-binding protein 1.

Techniques Used: Activation Assay, Expressing, Staining, Knock-Out, Activity Assay, Binding Assay

Illustration of the molecular mechanism of rifaximin in treating NASH in mice. Inhibition of the Helicobacter -DCA-Fxr-Hnf1a signalling pathway is required for rifaximin to ameliorate NASH in mice. DCA, deoxycholic acid; Fgf15, fibroblast growth factor 15; Fxr, farnesoid X receptor; Hnf1α, hepatocyte nuclear factor 1α; NASH, non-alcoholic steatohepatitis.

Figure Legend Snippet: Illustration of the molecular mechanism of rifaximin in treating NASH in mice. Inhibition of the Helicobacter -DCA-Fxr-Hnf1a signalling pathway is required for rifaximin to ameliorate NASH in mice. DCA, deoxycholic acid; Fgf15, fibroblast growth factor 15; Fxr, farnesoid X receptor; Hnf1α, hepatocyte nuclear factor 1α; NASH, non-alcoholic steatohepatitis.

Techniques Used: Inhibition

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Journal: Molecular Medicine Reports

Article Title: Study on the molecular mechanisms of rifaximin in the treatment of non‑alcoholic steatohepatitis based on the Helicobacter ‑DCA‑Fxr‑Hnf1α signalling pathway

doi: 10.3892/mmr.2024.13407

Figure Lengend Snippet: Rifaximin ameliorates non-alcoholic steatohepatitis in MCD diet-fed mice. (A) Photographs of livers in the MCS, MCD and MCD + rifaximin groups. (B) Liver weight, and liver weight to body weight ratio in each group. (C) Haematoxylin and eosin staining of livers in the MCS, MCD and MCD + rifaximin groups. Scale bars, 100 µm. (D) Steatosis score, hepatic ballooning score, interlobular inflammation score and NAS. (E) Oil red O staining of livers in the MCS, MCD and MCD + rifaximin groups. Scale bars, 100 µm. (F) Srebp1, Pparγ and CD36 mRNA expression levels in mouse livers. (G) Plasma ALT and AST levels in mice. n=8 mice/group. *P<0.05, **P<0.01, ***P<0.001, ****P<0.0001. ALT, alanine transaminase; AST, aspartate transaminase; MCD, methionine-choline deficient; MCS, methionine-choline sufficient; NAS, non-alcoholic fatty liver disease activity score; Srebp1, sterol regulatory element-binding protein 1.

Article Snippet: The mice in the MCD + rifaximin group were treated with rifaximin (MedChemExpress) by oral gavage (100 mg/kg/day) for 4 weeks ( ).

Techniques: Staining, Expressing, Clinical Proteomics, Activity Assay, Binding Assay

Journal: Molecular Medicine Reports

Article Title: Study on the molecular mechanisms of rifaximin in the treatment of non‑alcoholic steatohepatitis based on the Helicobacter ‑DCA‑Fxr‑Hnf1α signalling pathway

doi: 10.3892/mmr.2024.13407

Figure Lengend Snippet: Rifaximin alleviates liver fibrosis in mice with MCD diet-induced non-alcoholic steatohepatitis. (A) Sirius Red staining of livers in each group. Scale bars, 100 µm. (B) α-Sma immunostaining of livers in each group. Scale bars, 100 µm. (C) Col1a1 immunostaining of livers in each group. Scale bars, 100 µm. (D) α-Sma and Col1a1 mRNA expression levels of livers in each group. (E) Hydroxyproline content in mouse livers. n=8 mice/group. *P<0.05, **P<0.01, ***P<0.001. α-Sma, α-smooth muscle actin; Col1a1, collagen type 1 α1; MCD, methionine-choline deficient; MCS, methionine-choline sufficient.

Article Snippet: The mice in the MCD + rifaximin group were treated with rifaximin (MedChemExpress) by oral gavage (100 mg/kg/day) for 4 weeks ( ).

Techniques: Staining, Immunostaining, Expressing

Journal: Molecular Medicine Reports

Article Title: Study on the molecular mechanisms of rifaximin in the treatment of non‑alcoholic steatohepatitis based on the Helicobacter ‑DCA‑Fxr‑Hnf1α signalling pathway

doi: 10.3892/mmr.2024.13407

Figure Lengend Snippet: Rifaximin affects the gut microbiota in mice with MCD diet-induced non-alcoholic steatohepatitis. (A) Caecal OTU, Chao index, Simpson index and Shannon index of mice. (B) Separation of samples by MCS, MCD, and MCD with rifaximin gavage was observed via NMDS analysis. (C) Relative abundance of gut microbiota in caecal content identified by LEfSe bar analysis among MCS, MCD and MCD + rifaximin groups. (D) Heatmap of separation at the phylum level of mouse faecal microbiota among the MCS, MCD and MCD + rifaximin groups. (E) Significant difference in mouse faecal microbiota at the phylum level among the MCS, MCD and MCD + rifaximin groups. (F) Heatmap of separation at the genus level of mouse faecal microflora among the MCS, MCD and MCD + rifaximin groups. (G) Significant difference of mouse faecal microbiota at the genus level among the MCS, MCD and MCD + rifaximin groups. Clustering was performed using the Pearson measurement. *P<0.05, **P<0.01, ***P<0.001. LDA, linear discriminant analysis; MCD, methionine-choline deficient; MCS, methionine-choline sufficient; NMDS, non-metric multidimensional scaling; OTU, operational taxonomic unit.

Article Snippet: The mice in the MCD + rifaximin group were treated with rifaximin (MedChemExpress) by oral gavage (100 mg/kg/day) for 4 weeks ( ).

Techniques:

Journal: Molecular Medicine Reports

Article Title: Study on the molecular mechanisms of rifaximin in the treatment of non‑alcoholic steatohepatitis based on the Helicobacter ‑DCA‑Fxr‑Hnf1α signalling pathway

doi: 10.3892/mmr.2024.13407

Figure Lengend Snippet: Rifaximin suppresses the Helicobacter -DCA-Fxr signalling pathway in MCD diet-fed mice. (A) Correlation analysis of intestinal microflora and BAs in the distal ileum was investigated using nonparametric Spearman's test. (B) BA levels in the distal ileum of mice. (C) Total BAs, conjugated BAs/unconjugated BAs ratio, and primary BAs/second BAs ratio in the distal ileum of mice. (D) Expression levels of Fxr, Fgf15 and Shp in the distal ileum. (E) Expression levels of Cyp7a1, Cyp7b1, Cyp8b1, and Cyp27a1 mRNA in the liver. n=8 mice/group. *P<0.05, **P<0.01, ***P<0.001, ****P<0.0001. BA, bile acid; DCA, deoxycholic acid; Fgf15, fibroblast growth factor 15; Fxr, farnesoid X receptor; MCD, methionine-choline deficient; MCS, methionine-choline sufficient.

Article Snippet: The mice in the MCD + rifaximin group were treated with rifaximin (MedChemExpress) by oral gavage (100 mg/kg/day) for 4 weeks ( ).

Techniques: Expressing

Journal: Molecular Medicine Reports

Article Title: Study on the molecular mechanisms of rifaximin in the treatment of non‑alcoholic steatohepatitis based on the Helicobacter ‑DCA‑Fxr‑Hnf1α signalling pathway

doi: 10.3892/mmr.2024.13407

Figure Lengend Snippet: Anti-NASH effects of rifaximin are impaired in mice lacking gut microbiota. (A) Schematic illustration of the experimental design of intestinal decontamination in mice with NASH. (B) Haematoxylin and eosin staining of livers in the MCD, MCD + rifaximin, MCD + Abx and MCD + Abx + rifaximin groups. Scale bars, 100 µm. (C) Steatosis score, hepatic ballooning score, interlobular inflammation score and NAS. (D) Oil red O staining for livers of mice in each group. Scale bars, 100 µm. (E) Pparγ and Srebp1 protein expression levels in mouse livers. (F) α-Sma protein expression levels in the livers in each group. n=8 mice/group. *P<0.05, **P<0.01, ***P<0.001, ****P<0.0001. α-Sma, α-smooth muscle actin; MCD, methionine-choline deficient; MCS, methionine-choline sufficient; NASH, non-alcoholic steatohepatitis; NAS, non-alcoholic fatty liver disease activity score; Srebp1, sterol regulatory element-binding protein 1.

Article Snippet: The mice in the MCD + rifaximin group were treated with rifaximin (MedChemExpress) by oral gavage (100 mg/kg/day) for 4 weeks ( ).

Techniques: Staining, Expressing, Activity Assay, Binding Assay

Journal: Molecular Medicine Reports

Article Title: Study on the molecular mechanisms of rifaximin in the treatment of non‑alcoholic steatohepatitis based on the Helicobacter ‑DCA‑Fxr‑Hnf1α signalling pathway

doi: 10.3892/mmr.2024.13407

Figure Lengend Snippet: Activation of hepatic Hnf1α is required for rifaximin to ameliorate NASH in mice. (A) Hnf1α H-KO NASH mice were established. (B) Schematic illustration of the experimental design. (C) Hnf1α protein expression levels in the mouse livers of each group. (D) Haematoxylin and eosin staining of livers in each group. Scale bars, 100 µm. (E) Steatosis score, hepatic ballooning score, interlobular inflammation score and NAS. (F) Oil red O staining for livers of mice in each group. Scale bars, 100 µm. (G) Pparγ and Srebp1 protein expression levels in the livers of each group. (H) α-Sma protein expression level in the livers in each group. n=5 mice/group. α-Sma, α-smooth muscle actin; Hnf1α, hepatocyte nuclear factor 1α; Hnf1α f/f , floxed Hnf1α; Hnf1α H-KO , hepatocyte-specific Hnf1α knockout; MCD, methionine-choline deficient; MCS, methionine-choline sufficient; NASH, non-alcoholic steatohepatitis; NAS, non-alcoholic fatty liver disease activity score; Srebp1, sterol regulatory element-binding protein 1.

Article Snippet: The mice in the MCD + rifaximin group were treated with rifaximin (MedChemExpress) by oral gavage (100 mg/kg/day) for 4 weeks ( ).

Techniques: Activation Assay, Expressing, Staining, Knock-Out, Activity Assay, Binding Assay

Journal: Molecular Medicine Reports

Article Title: Study on the molecular mechanisms of rifaximin in the treatment of non‑alcoholic steatohepatitis based on the Helicobacter ‑DCA‑Fxr‑Hnf1α signalling pathway

doi: 10.3892/mmr.2024.13407

Figure Lengend Snippet: Illustration of the molecular mechanism of rifaximin in treating NASH in mice. Inhibition of the Helicobacter -DCA-Fxr-Hnf1a signalling pathway is required for rifaximin to ameliorate NASH in mice. DCA, deoxycholic acid; Fgf15, fibroblast growth factor 15; Fxr, farnesoid X receptor; Hnf1α, hepatocyte nuclear factor 1α; NASH, non-alcoholic steatohepatitis.

Article Snippet: The mice in the MCD + rifaximin group were treated with rifaximin (MedChemExpress) by oral gavage (100 mg/kg/day) for 4 weeks ( ).

Techniques: Inhibition

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