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ugt1a4 recombinant enzyme  (MedChemExpress)
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MedChemExpress ugt1a4 recombinant enzyme
<t>UGT1A4</t> mediated CDCA-3β-glucuronide excessed induces BA disorder diarrhea. A , B Secondary bile acids concentration and total bile acid concentration in the colon ( n = 8). C , D Proportion of tauro-conjugated bile acids and glycol-conjugated bile acids. E PCOA plot of bile acids on Bray-Curtis dissimilarity matrices ( n = 8). F , G Relative protein expression of FXR, BCL2, BAX, and NFκB-P65. H , I Histomorphology and its score. Scale bars, 100 μm. J Bile acid metabolites and enzymes in CDCA metabolism pathway. K Volcano analysis enriched CDCA-3β-glucuronide in the colon. L Content of CDCA-3β-glucuronide ( n = 8). M Content of UGT1A4 enzyme ( n = 8). N , O , P Correlation between UGT1A4 content and total bile acids level, FXR level, and BAX level. The differences between groups were compared using either student’s t-test or two-way analysis of variance (ANOVA) followed by Tukey’s test for multiple comparisons, and statistical significance was considered at P < 0.05. Data were represented as mean ± SEM, and exhibited * P < 0.05, ** P < 0.01, *** P < 0.001. Correlation played on spearman two-tailed test in 99% confidence interval
Ugt1a4 Recombinant Enzyme, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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UGT1A4 mediated CDCA-3β-glucuronide excessed induces BA disorder diarrhea. A , B Secondary bile acids concentration and total bile acid concentration in the colon ( n = 8). C , D Proportion of tauro-conjugated bile acids and glycol-conjugated bile acids. E PCOA plot of bile acids on Bray-Curtis dissimilarity matrices ( n = 8). F , G Relative protein expression of FXR, BCL2, BAX, and NFκB-P65. H , I Histomorphology and its score. Scale bars, 100 μm. J Bile acid metabolites and enzymes in CDCA metabolism pathway. K Volcano analysis enriched CDCA-3β-glucuronide in the colon. L Content of CDCA-3β-glucuronide ( n = 8). M Content of UGT1A4 enzyme ( n = 8). N , O , P Correlation between UGT1A4 content and total bile acids level, FXR level, and BAX level. The differences between groups were compared using either student’s t-test or two-way analysis of variance (ANOVA) followed by Tukey’s test for multiple comparisons, and statistical significance was considered at P < 0.05. Data were represented as mean ± SEM, and exhibited * P < 0.05, ** P < 0.01, *** P < 0.001. Correlation played on spearman two-tailed test in 99% confidence interval

Journal: Microbiome

Article Title: Microbiota governs host chenodeoxycholic acid glucuronidation to ameliorate bile acid disorder induced diarrhea

doi: 10.1186/s40168-024-02011-8

Figure Lengend Snippet: UGT1A4 mediated CDCA-3β-glucuronide excessed induces BA disorder diarrhea. A , B Secondary bile acids concentration and total bile acid concentration in the colon ( n = 8). C , D Proportion of tauro-conjugated bile acids and glycol-conjugated bile acids. E PCOA plot of bile acids on Bray-Curtis dissimilarity matrices ( n = 8). F , G Relative protein expression of FXR, BCL2, BAX, and NFκB-P65. H , I Histomorphology and its score. Scale bars, 100 μm. J Bile acid metabolites and enzymes in CDCA metabolism pathway. K Volcano analysis enriched CDCA-3β-glucuronide in the colon. L Content of CDCA-3β-glucuronide ( n = 8). M Content of UGT1A4 enzyme ( n = 8). N , O , P Correlation between UGT1A4 content and total bile acids level, FXR level, and BAX level. The differences between groups were compared using either student’s t-test or two-way analysis of variance (ANOVA) followed by Tukey’s test for multiple comparisons, and statistical significance was considered at P < 0.05. Data were represented as mean ± SEM, and exhibited * P < 0.05, ** P < 0.01, *** P < 0.001. Correlation played on spearman two-tailed test in 99% confidence interval

Article Snippet: In this study, 50 μM and 100 μM CDCA, 10 μM CDCA-3β-glucuronide, and 10 μM UGT1A4 recombinant enzyme (UGT1A4 RE) were used to treat IPEC-J2 for 12–24 h, 10 3 CFU/mL L . reuteri and 50 μM I3C were used to treated IPEC-J2 for 12 h. AHR antagonist (MCE, USA) were used to prevent AHR moving from the cytoplasm to the nucleus.

Techniques: Concentration Assay, Expressing, Two Tailed Test

Effects of UGT1A4 and CDCA-3β-glucuronide on FXR inhibition and apoptosis. A Mice were intraperitoneal injected CDCA-3β-glucuronide. B Fecal water index ( n = 3). C , D Histomorphology and its score. Scale bars, 100 μm. E , F Relative protein expressions of TNF-α and BAX ( n = 3). G Relative gene levels of IL-6 , IL-1β , and TNF-α ( n = 3). H ABX mice were received microbiota transplantation from healthy donors, BADD donors. I , J Histomorphology ( I ) and its score ( J ). Scale bars, 100 μm. K Relative protein expressions of TNF-α and BAX. L , M Nucleus location and intensity of FXR in the gut epithelium cells ( n = 3). Scale bars, 25 μm. The differences between groups were compared using either student’s t test or two-way analysis of variance (ANOVA) followed by Tukey’s test for multiple comparisons, and statistical significance was considered at P < 0.05. Data were represented as mean ± SEM, and exhibited * P < 0.05, ** P < 0.01, *** P < 0.001

Journal: Microbiome

Article Title: Microbiota governs host chenodeoxycholic acid glucuronidation to ameliorate bile acid disorder induced diarrhea

doi: 10.1186/s40168-024-02011-8

Figure Lengend Snippet: Effects of UGT1A4 and CDCA-3β-glucuronide on FXR inhibition and apoptosis. A Mice were intraperitoneal injected CDCA-3β-glucuronide. B Fecal water index ( n = 3). C , D Histomorphology and its score. Scale bars, 100 μm. E , F Relative protein expressions of TNF-α and BAX ( n = 3). G Relative gene levels of IL-6 , IL-1β , and TNF-α ( n = 3). H ABX mice were received microbiota transplantation from healthy donors, BADD donors. I , J Histomorphology ( I ) and its score ( J ). Scale bars, 100 μm. K Relative protein expressions of TNF-α and BAX. L , M Nucleus location and intensity of FXR in the gut epithelium cells ( n = 3). Scale bars, 25 μm. The differences between groups were compared using either student’s t test or two-way analysis of variance (ANOVA) followed by Tukey’s test for multiple comparisons, and statistical significance was considered at P < 0.05. Data were represented as mean ± SEM, and exhibited * P < 0.05, ** P < 0.01, *** P < 0.001

Article Snippet: In this study, 50 μM and 100 μM CDCA, 10 μM CDCA-3β-glucuronide, and 10 μM UGT1A4 recombinant enzyme (UGT1A4 RE) were used to treat IPEC-J2 for 12–24 h, 10 3 CFU/mL L . reuteri and 50 μM I3C were used to treated IPEC-J2 for 12 h. AHR antagonist (MCE, USA) were used to prevent AHR moving from the cytoplasm to the nucleus.

Techniques: Inhibition, Injection, Transplantation Assay

Amelioration of UGT mediated bile acid disorder by activating FXR-Sirt1-LKB1-P53 axis in mice. A Mice were randomly assigned to one of the four groups shown in ( A ), except from control group, treated with oral gavage with saline or FXR agonist, or injection with LKB1 inhibitor, subsequently these mice received 3% DSS daily drink. B Body weight changes ( n = 6). C Total bile acid concentration in the feces ( n = 6). D UGT1A4 enzyme content in the colon ( n = 6). E Histomorphology score ( n = 6). Scale bars, 200 μm. F , G Intensity of FXR and LKB1 in the colon were showed by Immunohistochemistry ( n = 3 ).Scale bars, 50 μm. (H) TUNEL + cell in the colon was counted ( n = 3). Scale bars, 20 μm. The differences between groups were compared using either student’s t-test or two-way analysis of variance (ANOVA) followed by Tukey’s test for multiple comparisons, and statistical significance was considered at P < 0.05. Data were represented as mean ± SEM, and exhibited * P < 0.05, ** P < 0.01, *** P < 0.001

Journal: Microbiome

Article Title: Microbiota governs host chenodeoxycholic acid glucuronidation to ameliorate bile acid disorder induced diarrhea

doi: 10.1186/s40168-024-02011-8

Figure Lengend Snippet: Amelioration of UGT mediated bile acid disorder by activating FXR-Sirt1-LKB1-P53 axis in mice. A Mice were randomly assigned to one of the four groups shown in ( A ), except from control group, treated with oral gavage with saline or FXR agonist, or injection with LKB1 inhibitor, subsequently these mice received 3% DSS daily drink. B Body weight changes ( n = 6). C Total bile acid concentration in the feces ( n = 6). D UGT1A4 enzyme content in the colon ( n = 6). E Histomorphology score ( n = 6). Scale bars, 200 μm. F , G Intensity of FXR and LKB1 in the colon were showed by Immunohistochemistry ( n = 3 ).Scale bars, 50 μm. (H) TUNEL + cell in the colon was counted ( n = 3). Scale bars, 20 μm. The differences between groups were compared using either student’s t-test or two-way analysis of variance (ANOVA) followed by Tukey’s test for multiple comparisons, and statistical significance was considered at P < 0.05. Data were represented as mean ± SEM, and exhibited * P < 0.05, ** P < 0.01, *** P < 0.001

Article Snippet: In this study, 50 μM and 100 μM CDCA, 10 μM CDCA-3β-glucuronide, and 10 μM UGT1A4 recombinant enzyme (UGT1A4 RE) were used to treat IPEC-J2 for 12–24 h, 10 3 CFU/mL L . reuteri and 50 μM I3C were used to treated IPEC-J2 for 12 h. AHR antagonist (MCE, USA) were used to prevent AHR moving from the cytoplasm to the nucleus.

Techniques: Control, Saline, Injection, Concentration Assay, Immunohistochemistry, TUNEL Assay

The important role of Lactobacillus reuteri in inhibiting UGT1A4 and its damages. A Shannon index of α diversity ( n = 8). B NMDS analysis of β diversity ( n = 8). C Proportion of bacteria in different groups ( n = 8). D Lesfe analysis for differential bacteria, orange represented healthy group, grey represented BADD group ( n = 8). E Correlation analysis between significant differential microflora and enriched metabolic pathways ( n = 8). F Relative abundance of Lactobacillus reuteri (P value = 0.00457) ( n = 8). G Correlation analysis between CDCA-3β-glucuronide content and possible bacteria, which could impact UGT1A4 enzyme ( n = 8). H L . reuteri was treated to enterocyte. (I) UGT1A4 content in enterocyte treated by L . reuteri ( n = 5). J , K Mice were received oral gavage with L . reuteri , and measured relative gene level of UGT1A4 ( n = 6 ). (L) Correlation analysis between faecal abundance of L . reuteri and UGT1A4 level ( n = 6). M Location and expression of NF-κB were showed by immunofluorescence. Scale bars, 200 μm. N , O Relative protein expressions of TNF-α, BAX, and Occludin ( n = 3). P Apoptosis associated signals were enriched by PICURST ( n = 8). The differences between groups were compared using either student’s t test or two-way analysis of variance (ANOVA) followed by Tukey’s test for multiple comparisons, and statistical significance was considered at P < 0.05. Data were represented as mean ± SEM, and exhibited * P < 0.05, ** P < 0.01, *** P < 0.001. Correlation played on spearman two-tailed test in 99% confidence interval

Journal: Microbiome

Article Title: Microbiota governs host chenodeoxycholic acid glucuronidation to ameliorate bile acid disorder induced diarrhea

doi: 10.1186/s40168-024-02011-8

Figure Lengend Snippet: The important role of Lactobacillus reuteri in inhibiting UGT1A4 and its damages. A Shannon index of α diversity ( n = 8). B NMDS analysis of β diversity ( n = 8). C Proportion of bacteria in different groups ( n = 8). D Lesfe analysis for differential bacteria, orange represented healthy group, grey represented BADD group ( n = 8). E Correlation analysis between significant differential microflora and enriched metabolic pathways ( n = 8). F Relative abundance of Lactobacillus reuteri (P value = 0.00457) ( n = 8). G Correlation analysis between CDCA-3β-glucuronide content and possible bacteria, which could impact UGT1A4 enzyme ( n = 8). H L . reuteri was treated to enterocyte. (I) UGT1A4 content in enterocyte treated by L . reuteri ( n = 5). J , K Mice were received oral gavage with L . reuteri , and measured relative gene level of UGT1A4 ( n = 6 ). (L) Correlation analysis between faecal abundance of L . reuteri and UGT1A4 level ( n = 6). M Location and expression of NF-κB were showed by immunofluorescence. Scale bars, 200 μm. N , O Relative protein expressions of TNF-α, BAX, and Occludin ( n = 3). P Apoptosis associated signals were enriched by PICURST ( n = 8). The differences between groups were compared using either student’s t test or two-way analysis of variance (ANOVA) followed by Tukey’s test for multiple comparisons, and statistical significance was considered at P < 0.05. Data were represented as mean ± SEM, and exhibited * P < 0.05, ** P < 0.01, *** P < 0.001. Correlation played on spearman two-tailed test in 99% confidence interval

Article Snippet: In this study, 50 μM and 100 μM CDCA, 10 μM CDCA-3β-glucuronide, and 10 μM UGT1A4 recombinant enzyme (UGT1A4 RE) were used to treat IPEC-J2 for 12–24 h, 10 3 CFU/mL L . reuteri and 50 μM I3C were used to treated IPEC-J2 for 12 h. AHR antagonist (MCE, USA) were used to prevent AHR moving from the cytoplasm to the nucleus.

Techniques: Bacteria, Expressing, Immunofluorescence, Two Tailed Test

Lactobacillus reuteri derived I3C reduces UGT1A4 mediated BA disorder by activating AHR. A AHR gene count of transcriptome sequencing in gut epithelial cells ( n = 3-7). B UGT1A4 enzyme content of gut epithelial cells treated with AHR antagonist ( n = 3). C Experiment of FMT mice with Lactobacillus reuteri administrated gavage. D PCOA plot of metabolities on bray-curtis dissimilarity matrices ( n = 3). E Venn plot at the range of level 1, VIP score > 1, and P value < 0.05, and the relative abundance of I3C ( n = 3 ). F , G , H Location and expression of AHR and UGT1A4 in gut epithelial cells treated with AHR antagonist, UGT1A4 recombinant enzyme, and I3C ( n = 3 ). (I) UGT1A4 enzyme content of gut epithelial cells treated with AHR antagonist and I3C ( n = 3). J FMT mice were given oral I3C and oral I3C combined with CDCA. (K) Histomorphology score ( n = 4–6). Scale bars, 100 μm. The differences between groups were compared using either student’s t test or two-way analysis of variance (ANOVA) followed by Tukey’s test for multiple comparisons, and statistical significance was considered at P < 0.05. Data were represented as mean ± SEM, and exhibited * P < 0.05, ** P < 0.01, *** P < 0.001

Journal: Microbiome

Article Title: Microbiota governs host chenodeoxycholic acid glucuronidation to ameliorate bile acid disorder induced diarrhea

doi: 10.1186/s40168-024-02011-8

Figure Lengend Snippet: Lactobacillus reuteri derived I3C reduces UGT1A4 mediated BA disorder by activating AHR. A AHR gene count of transcriptome sequencing in gut epithelial cells ( n = 3-7). B UGT1A4 enzyme content of gut epithelial cells treated with AHR antagonist ( n = 3). C Experiment of FMT mice with Lactobacillus reuteri administrated gavage. D PCOA plot of metabolities on bray-curtis dissimilarity matrices ( n = 3). E Venn plot at the range of level 1, VIP score > 1, and P value < 0.05, and the relative abundance of I3C ( n = 3 ). F , G , H Location and expression of AHR and UGT1A4 in gut epithelial cells treated with AHR antagonist, UGT1A4 recombinant enzyme, and I3C ( n = 3 ). (I) UGT1A4 enzyme content of gut epithelial cells treated with AHR antagonist and I3C ( n = 3). J FMT mice were given oral I3C and oral I3C combined with CDCA. (K) Histomorphology score ( n = 4–6). Scale bars, 100 μm. The differences between groups were compared using either student’s t test or two-way analysis of variance (ANOVA) followed by Tukey’s test for multiple comparisons, and statistical significance was considered at P < 0.05. Data were represented as mean ± SEM, and exhibited * P < 0.05, ** P < 0.01, *** P < 0.001

Article Snippet: In this study, 50 μM and 100 μM CDCA, 10 μM CDCA-3β-glucuronide, and 10 μM UGT1A4 recombinant enzyme (UGT1A4 RE) were used to treat IPEC-J2 for 12–24 h, 10 3 CFU/mL L . reuteri and 50 μM I3C were used to treated IPEC-J2 for 12 h. AHR antagonist (MCE, USA) were used to prevent AHR moving from the cytoplasm to the nucleus.

Techniques: Derivative Assay, Sequencing, Expressing, Recombinant

Graphical abstract. Apoptosis induced by diarrhea caused by BA metabolism disturbance is associated with gut microflora. L . reuteri derives I3C to activate AHR in gut epithelial cells to regulated host UGT1A4 enzyme to improve BA metabolism disorder diarrhea. Host UGT1A4 mediates CDCA glucuronidation to produce CDCA-3β-glucuronide to repress FXR activity. Inhibited FXR could not enter the nucleus to transcriptionally regulate SIRT1 mRNA, which reduces the deacetylation level of LKB1 protein. LKB1 is able to bind to P53 and competitively inhibit P53 activity, thereby inhibiting apoptosis, but anti-apoptotic ability of LKB1 is suppressed by decreased activity of FXR in BA metabolism disorder diarrhea

Journal: Microbiome

Article Title: Microbiota governs host chenodeoxycholic acid glucuronidation to ameliorate bile acid disorder induced diarrhea

doi: 10.1186/s40168-024-02011-8

Figure Lengend Snippet: Graphical abstract. Apoptosis induced by diarrhea caused by BA metabolism disturbance is associated with gut microflora. L . reuteri derives I3C to activate AHR in gut epithelial cells to regulated host UGT1A4 enzyme to improve BA metabolism disorder diarrhea. Host UGT1A4 mediates CDCA glucuronidation to produce CDCA-3β-glucuronide to repress FXR activity. Inhibited FXR could not enter the nucleus to transcriptionally regulate SIRT1 mRNA, which reduces the deacetylation level of LKB1 protein. LKB1 is able to bind to P53 and competitively inhibit P53 activity, thereby inhibiting apoptosis, but anti-apoptotic ability of LKB1 is suppressed by decreased activity of FXR in BA metabolism disorder diarrhea

Article Snippet: In this study, 50 μM and 100 μM CDCA, 10 μM CDCA-3β-glucuronide, and 10 μM UGT1A4 recombinant enzyme (UGT1A4 RE) were used to treat IPEC-J2 for 12–24 h, 10 3 CFU/mL L . reuteri and 50 μM I3C were used to treated IPEC-J2 for 12 h. AHR antagonist (MCE, USA) were used to prevent AHR moving from the cytoplasm to the nucleus.

Techniques: Activity Assay