Journal: British Journal of Pharmacology

Article Title: Tauroursodeoxycholic acid inhibits intestinal inflammation and barrier disruption in mice with non‐alcoholic fatty liver disease

doi: 10.1111/bph.14095

Figure Lengend Snippet: TUDCA attenuates HFD‐induced hepatic steatosis and inflammatory responses in NAFLD mice. (A, left) Representative macroscopic images of the livers of NCD, HFD and TUDCA mice, (A, middle) Liver weight and (A, right) the ratio of the liver weight and body weight of the three groups. (B, left) Representative H&E‐treated and Oil Red O‐stained sections in liver samples and (B, right) NAS of three groups. (C) The serum and hepatic TG and TC contents of mice in the indicated groups were measured using the elisa. (D) The mRNA expression levels of genes associated with fatty acid synthesis, transport and β‐oxidation, (E) inflammatory cytokines and (F) innate immunity components in the liver were detected by qPCR. The data are presented as the means ± SEM. One‐way ANOVA followed by Newman–Keuls post hoc test for multiple comparison. NCD group, n = 8; HFD group, n = 9; and HFD + TUDCA, n = 6. *P < 0.05. Hmgcr, 3‐hydroxy‐3‐methylglutaryl CoA reductase. ND, not detected.

Article Snippet: Both the normal chow diet (NCD) (containing 10% fat by energy) and high‐fat diet (HFD) (containing 60% fat by energy) were purchased from Beijing HFK Bio‐Technology Co., Ltd. (Beijing, China).

Techniques: Staining, Enzyme-linked Immunosorbent Assay, Expressing, Comparison

Journal: British Journal of Pharmacology

Article Title: Tauroursodeoxycholic acid inhibits intestinal inflammation and barrier disruption in mice with non‐alcoholic fatty liver disease

doi: 10.1111/bph.14095

Figure Lengend Snippet: TUDCA ameliorates HFD‐induced obesity and insulin resistance in NAFLD mice. (A, left) Representative macroscopic pictures and (A, right) body weight of the NCD, HFD and HFD + TUDCA groups. (B) Fasting glucose, (C) fasting insulin and (D) HOMA‐IR in mice treated with NCD, HFD or HFD + TUDCA. Fasting glucose and fasting insulin levels were measured at the endpoint of this experiment. HOMA‐IR was calculated as HOMA‐IR = (FBG (mM) × FINS (ng·mL−1))/22.5. (E) The IPGTT and (F) IPITT assays were performed to evaluate the insulin sensitivity of mice in the indicated groups treated with NCD, HFD or HFD + TUDCA. The data are presented as the mean ± SEM for (A–D) and mean ± SD for (E–F). One‐way ANOVA followed by Newman–Keuls post hoc test for multiple comparison. NCD group, n = 8; HFD group, n = 9; and HFD + TUDCA, n = 6. *P < 0.05 versus the NCD group; # P < 0.05 versus the HFD group.

Article Snippet: Both the normal chow diet (NCD) (containing 10% fat by energy) and high‐fat diet (HFD) (containing 60% fat by energy) were purchased from Beijing HFK Bio‐Technology Co., Ltd. (Beijing, China).

Techniques: Comparison

Journal: British Journal of Pharmacology

Article Title: Tauroursodeoxycholic acid inhibits intestinal inflammation and barrier disruption in mice with non‐alcoholic fatty liver disease

doi: 10.1111/bph.14095

Figure Lengend Snippet: TUDCA attenuates gut inflammation. (A) Representative ileum H&E staining sections (left panel) and corresponding histopathological score (right panel) in the NCD, HFD and HFD + TUDCA groups; (B, C) the mRNA expression levels of inflammatory cytokines and components of innate immune signalling were measured in the indicated groups; (D) the mRNA expression levels of inflammatory cytokines and components of innate immune signalling were measured in the indicated groups in Caco‐2 cells. CON, control group treated with vehicle; PA + LPS group, Caco‐2 cells co‐stimulated with 600 μM palmitate and 10 μg·mL−1 LPS for 6 h; PA + LPS + TUDCA group, Caco‐2 cells treated with the combination of palmitate (600 mΜ), LPS (10 μg·mL−1) and TUDCA (500 mM) for 6 h. The data are presented as the means ± SEM. One‐way ANOVA followed by the Newman–Keuls post hoc test for multiple comparisons. NCD group, n = 8; HFD group, n = 9; and HFD + TUDCA, n = 6. In vitro experiment, n = 5. *P < 0.05.

Article Snippet: Both the normal chow diet (NCD) (containing 10% fat by energy) and high‐fat diet (HFD) (containing 60% fat by energy) were purchased from Beijing HFK Bio‐Technology Co., Ltd. (Beijing, China).

Techniques: Staining, Expressing, Control, In Vitro

Journal: British Journal of Pharmacology

Article Title: Tauroursodeoxycholic acid inhibits intestinal inflammation and barrier disruption in mice with non‐alcoholic fatty liver disease

doi: 10.1111/bph.14095

Figure Lengend Snippet: TUDCA improves intestinal barrier function. (A) The mRNA levels of ileum tight junction molecules were measured by real‐time PCR. (B, C) The mRNA levels of gut mucin lysozyme, Iap, Muc2 and C3gnt in the mice of different groups were detected by qPCR. (D) The TEERs of the CON, PA + LPS and PA + LPS + TUDCA groups were detected in Caco‐2 cells. CON, control group treated with vehicle; PA + LPS group, Caco‐2 cells co‐stimulated with 600 μM palmitate and 10 μg·mL−1 LPS for the indicated times; PA + LPS + TUDCA group, Caco‐2 cells treated with the combination of palmitate (600 mΜ), LPS (10 μg·mL−1) and TUDCA (500 mM) for the indicated times. The data are presented as the means ± SEM. One‐way ANOVA followed by the Newman–Keuls post hoc test for multiple comparisons. NCD group, n = 8; HFD group, n = 9; and HFD + TUDCA, n = 6. *P < 0.05; in vitro experiment, n = 5. *P < 0.05 versus the CON group; # P < 0.05 versus the PA + LPS group.

Article Snippet: Both the normal chow diet (NCD) (containing 10% fat by energy) and high‐fat diet (HFD) (containing 60% fat by energy) were purchased from Beijing HFK Bio‐Technology Co., Ltd. (Beijing, China).

Techniques: Real-time Polymerase Chain Reaction, Control, In Vitro

Journal: British Journal of Pharmacology

Article Title: Tauroursodeoxycholic acid inhibits intestinal inflammation and barrier disruption in mice with non‐alcoholic fatty liver disease

doi: 10.1111/bph.14095

Figure Lengend Snippet: TUDCA suppresses gut lipid transport genes expression. (A) The mRNA levels of ileum lipid transport‐related genes (Cd36, Fabp, Fatp4 and Ffar3) in the NCD, HFD and HFD + TUDCA groups were measured. NCD group, n = 8; HFD group, n = 9; and HFD + TUDCA, n = 6. *P < 0.05. (B) The expression levels of ileum lipid transport‐related genes were detected in Caco‐2 cells (n = 5). CON, control group treated with vehicle; PA + LPS group, Caco‐2 cells co‐stimulated with 600 μM palmitate and 10 μg·mL−1 LPS for 6 h; PA + LPS + TUDCA group, Caco‐2 cells treated with the combination of palmitate (600 mΜ), LPS (10 μg·mL−1) and TUDCA (500 mM) for 6 h. The data are presented as the means ± SEM. One‐way ANOVA followed by the Newman–Keuls post hoc test for multiple comparisons. *P < 0.05.

Article Snippet: Both the normal chow diet (NCD) (containing 10% fat by energy) and high‐fat diet (HFD) (containing 60% fat by energy) were purchased from Beijing HFK Bio‐Technology Co., Ltd. (Beijing, China).

Techniques: Expressing, Control

Journal: British Journal of Pharmacology

Article Title: Tauroursodeoxycholic acid inhibits intestinal inflammation and barrier disruption in mice with non‐alcoholic fatty liver disease

doi: 10.1111/bph.14095

Figure Lengend Snippet: TUDCA treated mice show different gut microbiota composition compared with HFD‐fed mice. (A) PCoA score plot; PCoA score plot based on unweighted (left panel) and weighted (right panel) UniFrac metrics; (B) average phylum distribution of gut microbiomes in the NCD, HFD and HFD + TUDCA groups; and (C, D) comparison of the taxonomic abundance among the indicated groups. The data are presented as the means ± SEM. The statistical significance in bacterial composition among the different samples was assessed by the ANOSIM test. NCD group, n = 8; HFD group, n = 9; and HFD + TUDCA, n = 6. *P < 0.05.

Article Snippet: Both the normal chow diet (NCD) (containing 10% fat by energy) and high‐fat diet (HFD) (containing 60% fat by energy) were purchased from Beijing HFK Bio‐Technology Co., Ltd. (Beijing, China).

Techniques: Comparison