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Bruschettini SRL
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DuPont de Nemours
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Merck & Co
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Santa Cruz Biotechnology
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Shanghai Yuanye Biochemicals
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MedChemExpress
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MedChemExpress
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Biosynth Carbosynth
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Selleck Chemicals
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Image Search Results
Journal: Diabetes
Article Title: Tauroursodeoxycholic Acid May Improve Liver and Muscle but Not Adipose Tissue Insulin Sensitivity in Obese Men and Women
doi: 10.2337/db10-0308
Figure Lengend Snippet: Subjects' characteristics, metabolic variables, and body composition
Article Snippet: Both
Techniques: Clinical Proteomics
Journal: Diabetes
Article Title: Tauroursodeoxycholic Acid May Improve Liver and Muscle but Not Adipose Tissue Insulin Sensitivity in Obese Men and Women
doi: 10.2337/db10-0308
Figure Lengend Snippet: Liver, muscle, and adipose tissue insulin sensitivity before (□) and after ( ) 4 weeks of placebo or TUDCA treatment. A : Hepatic insulin sensitivity index. B : Glucose rate of disappearance ( R d ); data represent only 8 of 10 subjects who received TUDCA treatment because of technical difficulties in obtaining blood samples in two subjects. C : Palmitate rate of appearance. Values are means ± SD. *Value significantly different from corresponding value before treatment, P < 0.05. †Main effect of insulin, P < 0.0001.
Article Snippet: Both
Techniques:
Journal: Diabetes
Article Title: Tauroursodeoxycholic Acid May Improve Liver and Muscle but Not Adipose Tissue Insulin Sensitivity in Obese Men and Women
doi: 10.2337/db10-0308
Figure Lengend Snippet: Effect of placebo (□) or TUDCA ( ) treatment on skeletal muscle IRS Tyr , Akt Ser473 , and JNK Thr183/Tyr185 levels. Values are means ± SD and expressed relative to values before treatment, which were set to one for each person. *Value significantly different from corresponding placebo value, P < 0.05.
Article Snippet: Both
Techniques:
Journal: Diabetes
Article Title: Tauroursodeoxycholic Acid May Improve Liver and Muscle but Not Adipose Tissue Insulin Sensitivity in Obese Men and Women
doi: 10.2337/db10-0308
Figure Lengend Snippet: Endoplasmic reticulum stress markers before (□) and after ( ) placebo or TUDCA therapy. A : Gene expression (relative to 18S rRNA). B : Protein content (relative to actin). Values are medians and quartiles.
Article Snippet: Both
Techniques: Gene Expression
Journal: Purinergic Signalling
Article Title: Bile acids are potent inhibitors of rat P2X2 receptors
doi: 10.1007/s11302-019-09657-2
Figure Lengend Snippet: Bile acids inhibit rat P2X2 at micromolar concentrations. a Representative current traces of Xenopus laevis oocytes expressing rat P2X2; P2X2 was activated by ATP (10 μM, black bar). Blue bars indicate the addition of 20 μM of different bile acids or control (solution exchange only). b Mean current amplitudes in the presence of the indicated substance relative to the ATP-activated current prior to substance application. Error bars represent standard error of the mean (S.E.M.), **p < 0.005, ***p < 0.001; n = 7–11. c Structure of TLCA with its conjugated taurine group indicated in gray. Hydroxy groups at the three carbon atoms highlighted by their IUPAC number discriminate the tested bile acids. The hydroxyl groups of each bile acid with their steric orientation are summarized in the table. TLCA, taurolithocholic acid; TCDCA, taurochenodeoxycholic acid; TUDCA, tauroursodeoxycholic acid; TDCA, taurodeoxycholic acid; TCA, taurocholic acid; THDCA, taurohydodeoxycholic acid. d Representative current trace of rat P2X2 activated by ATP (10 μM, black bar). Blue bars indicate the application of 20 μM of different bile acids alone
Article Snippet:
Techniques: Expressing, Control
Journal: Nature Communications
Article Title: Diet-induced RKIP downregulation disrupts PC/PE-ER homeostasis to drive MASLD
doi: 10.1038/s41467-025-65982-8
Figure Lengend Snippet: a Western blotting analysis of RKIP expression in PA-stimulated HepG2 cells with CHX (100 μg/mL), CQ (100 μM) or MG132 (10 μM) treatment for 12 hrs. b Western blotting analysis of RKIP expression in TM (1.2 μM) or Tha (100 nM)-stimulated HepG2 cells with CHX, MG132 or CQ treatment for 6 hrs. c Western blotting analysis of RKIP expression in PA-stimulated HepG2 cells treated with TUDCA (1 mM) or Vehicle (Veh) for the indicated times. d , e Western blotting analysis of RKIP expression in HepG2 ( d ) and HeLa cells ( e ) treated with PA, PA plus CB-5083 (2.5 μM) or Vehicle for 12 hrs. f , g Anti-VCP Co-Immunoprecipitation (Co-IP) of the interaction between VCP and RKIP in HepG2 ( f ) and HeLa cells ( g ) with or without PA stimulation for 12 hrs. h Acyl-biotin exchange (ABE) assays measuring the acylation levels of RKIP-flag in transfected HepG2 cells with or without PA stimulation for 12 hrs. i The acylation levels of RKIP-flag in transfected HepG2 cells with PA (12 hrs), PA plus TUDCA (12 hrs) or Tha (6 hrs) treatment. j The acylation levels of RKIP-flag, RKIP C133A -flag and RKIP C168A -flag in transfected HEK293T cells. k Western blotting analysis of RKIP-flag, RKIP C133A -flag and RKIP C168A -flag in transfected HEK293T cells with or without MG132 treatment for 12 hrs. l Anti-flag Co-IP of the interaction between RKIP-flag, RKIP C133A -flag or RKIP C168A -flag and VCP in transfected HEK293T cells in the presence of MG132. m Anti-GFP Co-IP of the interaction between ZDHHC4 -GFP (left) or ZDHHC6-GFP (right) and RKIP-flag in co-transfected HEK293T cells treated with PA (12 hrs), PA plus TUCDA (12 hrs), Tha (6 hrs) or TM (6 hrs) in the presence of MG132. n Anti-flag Co-IP of the interaction between RKIP-flag and ZDHHC3/4/6 in RKIP-flag-overexpressed HepG2 cells with or without PA stimulation for 12 hrs in the presence of MG132. Numbers below the blot indicate the results of densitometric analysis of RKIP relative to GAPDH ( a-e , k ). Data are representative of at least two independent experiments. Source data are provided as a Source Data file .
Article Snippet: For TUDCA treatment, HFD-fed mice were injected with
Techniques: Western Blot, Expressing, Immunoprecipitation, Co-Immunoprecipitation Assay, Transfection
Journal: Nature Communications
Article Title: Diet-induced RKIP downregulation disrupts PC/PE-ER homeostasis to drive MASLD
doi: 10.1038/s41467-025-65982-8
Figure Lengend Snippet: a , b Western blotting ( a ) and quantitative analysis ( b ) of ER stress markers in liver of CD- or HFD-fed RKIP f/f and Alb cre RKIP f/f mice (CD groups, n = 3; HFD groups, n = 4). c , d Western blotting analysis of ER stress markers in WT and RKIP knockout (KO) HepG2 ( c ) and HeLa cells ( d ) with PA stimulation for the indicated times. e Representative fluorescence images of LDs (upper), the percentage of LDs (bottom left, n = 3) and the mean number of LDs per cell (bottom right, n = 20) in WT and KO primary hepatocytes treated with PA, TUDCA, PA plus TUDCA or Vehicle for 24 hrs. Scale bars, 40 μm. f RKIP f/f and Alb cre RKIP f/f mice were fed with HFD for 16 weeks and treated with TUDCA (250 mg/kg/day, i.p.) for the last 4 weeks. (Vehicle, n = 3 per group, TUDCA n = 5 per group) Representative H&E staining, Oil red O staining and Masson staining of the liver tissues. Representative 3 liver sections from 3 mice per group. Scale bars, 200 μm. g Quantification for the LDs percentage of liver sections as described in f . h , i The levels of serum ALT ( h ), hepatic total cholesterol (TC) and triglyceride (TG) ( i ) of HFD-fed and TUDCA-treated RKIP f/f and Alb cre RKIP f/f mice as described in f . Data are presented as mean ± SEM ( b, e, g-i ). * p < 0.05, ** p < 0.01, *** p < 0.001. Each dot represents a biological replicate ( b, g-i ) or a technical replicate ( e ). P values were calculated by two-tailed unpaired Student’s t -tests in ( b, e ) and one-way ANOVA in ( g-i ). The samples were derived from the same experiment, pIRE1, RKIP and GAPDH were probed on the same gel, and IRE1, pPERK, PERK, pEIF2α, EIF2α, p-p65, p65, pERK1/2 and ERK1/2 were processed on separate gels in parallel in ( a, c, d ). Numbers below the blot indicate the results of densitometric analysis of the phosphorylated protein relative to the total protein (P/T) and the indicated protein relative to GAPDH (/GAPDH) ( c, d ). Data are representative of at least two independent experiments. Source data are provided as a Source Data file .
Article Snippet: For TUDCA treatment, HFD-fed mice were injected with
Techniques: Western Blot, Knock-Out, Fluorescence, Staining, Two Tailed Test, Derivative Assay
Journal: Nutrients
Article Title: FXR, a Key Regulator of Lipid Metabolism, Is Inhibited by ER Stress-Mediated Activation of JNK and p38 MAPK in Large Yellow Croakers ( Larimichthys crocea ) Fed High Fat Diets
doi: 10.3390/nu13124343
Figure Lengend Snippet: Effects of HFD and ER stress on the expression of FXR in large yellow croaker: ( A , B ) Immunoblots or qRT-PCR assays for FXR and ER stress markers in the liver of large yellow croakers fed HFD diet; ( C – F ) immunoblots or qRT-PCR assays for FXR and ER stress markers in LYCL cells after PA, TG, or TM treatment; ( G ) immunoblots for FXR in LYCL cells after TUDCA treatment. Data are shown as means ± SEMs ( n = 3) and were analyzed using Student’s t -test, * p < 0.05.
Article Snippet: The LYCL cells were treated for 24 h with palmitic acid (PA, 100 μM, Sigma, St. Louis, MO, USA), thapsigargin (TG, 1 μM, MCE, Bloomfield, NJ, USA), tunicamycin (TM, 4 μM, MCE, Bloomfield, NJ, USA) and
Techniques: Expressing, Western Blot, Quantitative RT-PCR
Journal: Cellular and Molecular Gastroenterology and Hepatology
Article Title: The Food Additive Maltodextrin Promotes Endoplasmic Reticulum Stress–Driven Mucus Depletion and Exacerbates Intestinal Inflammation
doi: 10.1016/j.jcmgh.2018.09.002
Figure Lengend Snippet: ER stress inhibition reduces MDX-mediated Ern-2 up-regulation and improves colitis in MDX-fed mice. ( A ) HT29-MTX cells were pretreated with TUDCA (10 μmol/L) or dimethyl sulfoxide (vehicle) and then stimulated with MDX for 1 hour. Ern-2 RNA transcripts were analyzed by real-time PCR. Data are means ± SD of 4 independent experiments. Differences between groups were compared using the 2-tailed Student t test (* P ≤ .05). ( B and C ) Wild-type mice were exposed to drinking water supplemented with 5% MDX for 45 days and injected or not with TUDCA (250 mg/kg intraperitoneally) every other day starting from day 21. Mice were killed on day 45, colonic tissues were isolated, and ( B ) Ern-2 , Ern-1 , and Xbp1s RNA transcripts and ( C ) Muc-2 protein expression were evaluated by real-time PCR and immunofluorescence, respectively. ( B ) Data were generated using 7–10 mice per group from 3 independent experiments. Each point in the graph indicates the RNA expression of the specific transcript in the colon of a single mouse; horizontal bars indicate median value. Differences between groups were compared using the Mann–Whitney U test (* P ≤ .05). ( C ) Pictures are representative of 4 separate experiments in which similar results were obtained. Scale bars : 25 μm. ( D ) Wild-type mice were exposed to drinking water supplemented with 5% MDX for 45 days and injected or not with TUDCA (250 mg/kg intraperitoneally) every other day starting from day 21. Mice were exposed to 1.75% DSS to induce colitis starting from day 35 until death (day 45), and body weight was recorded every other day. Data were generated using 8–9 mice per group from 3 independent experiments and expressed as means ± SEM. Differences among groups were compared using 1-way analysis of variance followed by the Bonferroni post hoc test (** P ≤ .01). ( E and F ) Representative H&E staining of colon sections of mice treated as indicated in panel D and killed on day 45. ( F ) Scatter plot shows the histologic score. Data were generated using 8–9 mice per group from 3 independent experiments and expressed as means ± SD. Differences among groups were compared using 1-way analysis of variance followed by the Bonferroni post hoc test (* P ≤ .05; ** P ≤ .01). ( G and H ) Representative scatter plots showing ( G ) IL1β and ( H ) Lcn-2 RNA expression in colon tissues taken from mice treated as indicated in panel D and killed on day 45. Each point in the graph indicates the RNA expression of the specific transcript in the colon of a single mouse; horizontal bars indicate median value or means ± SD. Data were generated using 8–9 mice per group from 3 independent experiments. Differences among groups were compared using the Kruskal–Wallis test or 1-way analysis of variance followed by the Bonferroni post hoc test (* P ≤ .05). DAPI, 4′,6-diamidino-2-phenylindole; mRNA, messenger RNA.
Article Snippet: In parallel, mice receiving a MDX-enriched diet, together with control mice, were given 250 mg/kg
Techniques: Inhibition, Real-time Polymerase Chain Reaction, Injection, Isolation, Expressing, Immunofluorescence, Generated, RNA Expression, MANN-WHITNEY, Staining
Journal: Cellular and Molecular Gastroenterology and Hepatology
Article Title: The Food Additive Maltodextrin Promotes Endoplasmic Reticulum Stress–Driven Mucus Depletion and Exacerbates Intestinal Inflammation
doi: 10.1016/j.jcmgh.2018.09.002
Figure Lengend Snippet: Effect of MDX on mucosa-associated microbiota. ( A and B ) Wild-type mice were exposed to drinking water supplemented with 5% MDX for 45 days and injected or not with TUDCA (250 mg/kg intraperitoneally) every other day starting from day 21. Control mice received drinking water for 45 days. All mice were killed on day 45. ( A ) Relative abundance of phyla and classes are represented for colonic mucosa-associated microbiota. Horizontal bars indicate median value. Data were generated using 4–7 mice per group from 2 independent experiments. Differences among groups were compared using the Kruskal–Wallis test (* P ≤ .05). ( B ) Principal coordinates analysis (PCoA) of the unweighted and weighted UniFrac distance matrix of mucosa-associated bacteria from mice treated as indicated in panel A .
Article Snippet: In parallel, mice receiving a MDX-enriched diet, together with control mice, were given 250 mg/kg
Techniques: Injection, Control, Generated, Bacteria