cholestyramine resin Search Results


93
MedChemExpress cholestyramine resin
MWD promotes colitis development in their progeny by producing DCA. a As shown in Fig. a, WT mice ( n = 5) were colonized with gut microbiota from the W-N and N-N groups. Then, the concentration of DCA in the mice’s feces was measured using an ELISA assay kit. b – g <t>Cholestyramine</t> resin (resin) was given to mice in the W-N and N-N groups ( n = 6 per group) for 5 days to eliminate intestinal bile acids. Following that, mice were given TNBS to induce colitis. c Body weight changes in mice were evaluated daily after TNBS treatment. d Representative images of TNBS-treated colon in N-N+resin and W-N+resin groups. e The mice were sacrificed on day 4, and the colon length was recorded. f , g Histopathological analysis of colon sections. f Histological scores of colitis were assessed. g Representative images of the H&E-stained colon sections of relevant groups (scale bars 100 μm). a , c , e , and f Data represent means ± SEM; NS, not significant; ** P < 0.01; by unpaired Student’s t test. The data shown are representative of three independent experiments
Cholestyramine Resin, 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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Rohm and Haas the chloride salt of cholestyramine resin usp, sold as amberlite irp-276™
MWD promotes colitis development in their progeny by producing DCA. a As shown in Fig. a, WT mice ( n = 5) were colonized with gut microbiota from the W-N and N-N groups. Then, the concentration of DCA in the mice’s feces was measured using an ELISA assay kit. b – g <t>Cholestyramine</t> resin (resin) was given to mice in the W-N and N-N groups ( n = 6 per group) for 5 days to eliminate intestinal bile acids. Following that, mice were given TNBS to induce colitis. c Body weight changes in mice were evaluated daily after TNBS treatment. d Representative images of TNBS-treated colon in N-N+resin and W-N+resin groups. e The mice were sacrificed on day 4, and the colon length was recorded. f , g Histopathological analysis of colon sections. f Histological scores of colitis were assessed. g Representative images of the H&E-stained colon sections of relevant groups (scale bars 100 μm). a , c , e , and f Data represent means ± SEM; NS, not significant; ** P < 0.01; by unpaired Student’s t test. The data shown are representative of three independent experiments
The Chloride Salt Of Cholestyramine Resin Usp, Sold As Amberlite Irp 276™, supplied by Rohm and Haas, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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90
Purolite Life Sciences cholestyramine
MWD promotes colitis development in their progeny by producing DCA. a As shown in Fig. a, WT mice ( n = 5) were colonized with gut microbiota from the W-N and N-N groups. Then, the concentration of DCA in the mice’s feces was measured using an ELISA assay kit. b – g <t>Cholestyramine</t> resin (resin) was given to mice in the W-N and N-N groups ( n = 6 per group) for 5 days to eliminate intestinal bile acids. Following that, mice were given TNBS to induce colitis. c Body weight changes in mice were evaluated daily after TNBS treatment. d Representative images of TNBS-treated colon in N-N+resin and W-N+resin groups. e The mice were sacrificed on day 4, and the colon length was recorded. f , g Histopathological analysis of colon sections. f Histological scores of colitis were assessed. g Representative images of the H&E-stained colon sections of relevant groups (scale bars 100 μm). a , c , e , and f Data represent means ± SEM; NS, not significant; ** P < 0.01; by unpaired Student’s t test. The data shown are representative of three independent experiments
Cholestyramine, supplied by Purolite Life Sciences, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Rohm and Haas pharmaceutical grade cholestyramine resin
MWD promotes colitis development in their progeny by producing DCA. a As shown in Fig. a, WT mice ( n = 5) were colonized with gut microbiota from the W-N and N-N groups. Then, the concentration of DCA in the mice’s feces was measured using an ELISA assay kit. b – g <t>Cholestyramine</t> resin (resin) was given to mice in the W-N and N-N groups ( n = 6 per group) for 5 days to eliminate intestinal bile acids. Following that, mice were given TNBS to induce colitis. c Body weight changes in mice were evaluated daily after TNBS treatment. d Representative images of TNBS-treated colon in N-N+resin and W-N+resin groups. e The mice were sacrificed on day 4, and the colon length was recorded. f , g Histopathological analysis of colon sections. f Histological scores of colitis were assessed. g Representative images of the H&E-stained colon sections of relevant groups (scale bars 100 μm). a , c , e , and f Data represent means ± SEM; NS, not significant; ** P < 0.01; by unpaired Student’s t test. The data shown are representative of three independent experiments
Pharmaceutical Grade Cholestyramine Resin, supplied by Rohm and Haas, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Dow Chemical cholestyramine resin usp
FTIR spectra of DFS, <t>Duolite</t> TM AP 143/1083 (IR) and DFS:IR complex.
Cholestyramine Resin Usp, supplied by Dow Chemical, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Dow Chemical bile acid sequestrant cholestyramine resin
Mice (129/SvJ) receiving chow containing <t>cholestyramine</t> resin or control chow were pre-treated with streptomycin and infected with an equal mixture of the S. Typhimurium wild type and a fepE mutant. (A) Competitive indices recovered from feces over time. (B) Competitive indices recovered from colon contents. (C) Determination of concentrations of total bile acids in colon contents. (A–C) Bars represent geometric means ± standard error. *, P <0.05; **, P <0.01. (D) Combined histopathology score of pathological changes observed in sections from the cecum. Lines represent averages. Each circle or diamond represents the combined histopathology score from an individual animal. (E) Representative images of histopathological changes.
Bile Acid Sequestrant Cholestyramine Resin, supplied by Dow Chemical, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Boryung Inc cholestyramine resin 4 g/9 g
Classification of drugs
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Shanghai Yuanye Biochemicals cholestyramine resin
Bile acid (BA), which is an important functional component in Pien Tze Huang (PZH), regulates activation of the G protein-coupled bile acid receptor 1 (TGR5)-signal transducer and activator of transcription 3 (STAT3)-A20 signalling pathway. (A) Total BA levels were detected in the PZH solution and PZH plus <t>cholestyramine</t> resin. (B) Liquid chromatography-mass spectrometry (LC-MS) analysis of PZH supernatant treated with or without cholestyramine resin. (C) Peritoneal macrophages were pretreated with PZH (1.25 mg/mL) or cholestyramine resin-treated PZH (1.25 mg/mL) for 2 h, and then treated with lipopolysaccharide (LPS) (100 ng/mL) for 40 min. PZH treated with cholestyramine resin did not increase the protein expression of TGR5, phospho-STAT3 (p-STAT3) and A20 or decrease the protein expression of phospho-p65 (p-p65), phospho-extracellular signal-regulated kinases (p-ERK), and phosphor-C-Jun N-terminal kinases (p-JNK) induced by LPS. (D) Peritoneal macrophages were pretreated with PZH (1.25 mg/mL) or cholestyramine resin-treated PZH (1.25 mg/mL) for 2 h and then treated with LPS (100 ng/mL) for 6 h. PZH treated with cholestyramine resin did not decrease the mRNA levels of interleukin (IL)-6, tumour necrosis factor-α (TNF-α) and IL-1β induced by LPS. (E) The composition of BAs in the PZH solution was detected by LC-MS. (F) Peritoneal macrophages were pretreated with PZH (1.25 mg/mL), cholestyramine resin-treated PZH (1.25 mg/mL), and cholestyramine resin-treated PZH (1.25 mg/mL) + BAs for 2 h, respectively, and then treated with LPS (100 ng/mL) for 6 h. Replenishing BAs including cholic acid (CA) (61.53 μM), deoxycholic acid (DCA) (27.25 μM), chenodexycholic acid (9.75 μM), taurocholic acid (TCA) (20.52 μM), glycocholic acid (GCA) (7.466 μM) and lithocholic acid (LCA) (0.413 μM) in PZH after treatment with cholestyramine resin decreased the mRNA levels of TNF-α and IL-1β induced by LPS. (G) Peritoneal macrophages were pretreated with PZH (1.25 mg/mL), cholestyramine resin-treated PZH (1.25 mg/mL), and cholestyramine resin-treated PZH (1.25 mg/mL) + BAs for 2 h and then treated with LPS (100 ng/mL) for 40 min . Replenishing BAs including CA (61.53 μM), DCA (27.25 μM), chenodexycholic acid (9.75 μM), TCA (20.52 μM), GCA (7.466 μM) and LCA (0.413 μM) in PZH after treatment with cholestyramine resin decreased the expression of p-p65 and p-ERK induced by LPS. (H) Schematic model of the mechanism by which PZH attenuates the LPS-induced inflammatory response by activating TGR5-STAT3-A20 signalling pathway. PZH stimulates the phosphorylation of STAT3, which acts as a transcriptional activator for A20 to increase the expression of A20. A20 inhibits the activation of the nuclear factor-kappa B (NF-κB) and mitogen-activated protein kinase (MAPK) signalling pathways to decrease the production of proinflammatory cytokines to attenuate the sepsis progression. The results are representative of one of three experiments. The data are shown as the mean ± standard deviation (SD). ∗∗ P < 0.01, ∗∗∗ P < 0.001, ns: no significance, based on one-way analysis of variance (ANOVA) and two-tailed Student's t -test. CHOL: cholestyramine resin; TRAF6: tumor necrosis factor receptor-associated factor 6; IKK: nuclear factor- kappa B kinase; TAK1: transforming growth factor beta-activated kinase 1; IκBα: nuclear factor-kappa B inhibitor alpha.
Cholestyramine Resin, supplied by Shanghai Yuanye Biochemicals, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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90
Bristol Myers cholestyramine resin locholest
Bile acid (BA), which is an important functional component in Pien Tze Huang (PZH), regulates activation of the G protein-coupled bile acid receptor 1 (TGR5)-signal transducer and activator of transcription 3 (STAT3)-A20 signalling pathway. (A) Total BA levels were detected in the PZH solution and PZH plus <t>cholestyramine</t> resin. (B) Liquid chromatography-mass spectrometry (LC-MS) analysis of PZH supernatant treated with or without cholestyramine resin. (C) Peritoneal macrophages were pretreated with PZH (1.25 mg/mL) or cholestyramine resin-treated PZH (1.25 mg/mL) for 2 h, and then treated with lipopolysaccharide (LPS) (100 ng/mL) for 40 min. PZH treated with cholestyramine resin did not increase the protein expression of TGR5, phospho-STAT3 (p-STAT3) and A20 or decrease the protein expression of phospho-p65 (p-p65), phospho-extracellular signal-regulated kinases (p-ERK), and phosphor-C-Jun N-terminal kinases (p-JNK) induced by LPS. (D) Peritoneal macrophages were pretreated with PZH (1.25 mg/mL) or cholestyramine resin-treated PZH (1.25 mg/mL) for 2 h and then treated with LPS (100 ng/mL) for 6 h. PZH treated with cholestyramine resin did not decrease the mRNA levels of interleukin (IL)-6, tumour necrosis factor-α (TNF-α) and IL-1β induced by LPS. (E) The composition of BAs in the PZH solution was detected by LC-MS. (F) Peritoneal macrophages were pretreated with PZH (1.25 mg/mL), cholestyramine resin-treated PZH (1.25 mg/mL), and cholestyramine resin-treated PZH (1.25 mg/mL) + BAs for 2 h, respectively, and then treated with LPS (100 ng/mL) for 6 h. Replenishing BAs including cholic acid (CA) (61.53 μM), deoxycholic acid (DCA) (27.25 μM), chenodexycholic acid (9.75 μM), taurocholic acid (TCA) (20.52 μM), glycocholic acid (GCA) (7.466 μM) and lithocholic acid (LCA) (0.413 μM) in PZH after treatment with cholestyramine resin decreased the mRNA levels of TNF-α and IL-1β induced by LPS. (G) Peritoneal macrophages were pretreated with PZH (1.25 mg/mL), cholestyramine resin-treated PZH (1.25 mg/mL), and cholestyramine resin-treated PZH (1.25 mg/mL) + BAs for 2 h and then treated with LPS (100 ng/mL) for 40 min . Replenishing BAs including CA (61.53 μM), DCA (27.25 μM), chenodexycholic acid (9.75 μM), TCA (20.52 μM), GCA (7.466 μM) and LCA (0.413 μM) in PZH after treatment with cholestyramine resin decreased the expression of p-p65 and p-ERK induced by LPS. (H) Schematic model of the mechanism by which PZH attenuates the LPS-induced inflammatory response by activating TGR5-STAT3-A20 signalling pathway. PZH stimulates the phosphorylation of STAT3, which acts as a transcriptional activator for A20 to increase the expression of A20. A20 inhibits the activation of the nuclear factor-kappa B (NF-κB) and mitogen-activated protein kinase (MAPK) signalling pathways to decrease the production of proinflammatory cytokines to attenuate the sepsis progression. The results are representative of one of three experiments. The data are shown as the mean ± standard deviation (SD). ∗∗ P < 0.01, ∗∗∗ P < 0.001, ns: no significance, based on one-way analysis of variance (ANOVA) and two-tailed Student's t -test. CHOL: cholestyramine resin; TRAF6: tumor necrosis factor receptor-associated factor 6; IKK: nuclear factor- kappa B kinase; TAK1: transforming growth factor beta-activated kinase 1; IκBα: nuclear factor-kappa B inhibitor alpha.
Cholestyramine Resin Locholest, supplied by Bristol Myers, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Bristol Myers bile-acid-binding resins cholestyramine questran light
Bile acid (BA), which is an important functional component in Pien Tze Huang (PZH), regulates activation of the G protein-coupled bile acid receptor 1 (TGR5)-signal transducer and activator of transcription 3 (STAT3)-A20 signalling pathway. (A) Total BA levels were detected in the PZH solution and PZH plus <t>cholestyramine</t> resin. (B) Liquid chromatography-mass spectrometry (LC-MS) analysis of PZH supernatant treated with or without cholestyramine resin. (C) Peritoneal macrophages were pretreated with PZH (1.25 mg/mL) or cholestyramine resin-treated PZH (1.25 mg/mL) for 2 h, and then treated with lipopolysaccharide (LPS) (100 ng/mL) for 40 min. PZH treated with cholestyramine resin did not increase the protein expression of TGR5, phospho-STAT3 (p-STAT3) and A20 or decrease the protein expression of phospho-p65 (p-p65), phospho-extracellular signal-regulated kinases (p-ERK), and phosphor-C-Jun N-terminal kinases (p-JNK) induced by LPS. (D) Peritoneal macrophages were pretreated with PZH (1.25 mg/mL) or cholestyramine resin-treated PZH (1.25 mg/mL) for 2 h and then treated with LPS (100 ng/mL) for 6 h. PZH treated with cholestyramine resin did not decrease the mRNA levels of interleukin (IL)-6, tumour necrosis factor-α (TNF-α) and IL-1β induced by LPS. (E) The composition of BAs in the PZH solution was detected by LC-MS. (F) Peritoneal macrophages were pretreated with PZH (1.25 mg/mL), cholestyramine resin-treated PZH (1.25 mg/mL), and cholestyramine resin-treated PZH (1.25 mg/mL) + BAs for 2 h, respectively, and then treated with LPS (100 ng/mL) for 6 h. Replenishing BAs including cholic acid (CA) (61.53 μM), deoxycholic acid (DCA) (27.25 μM), chenodexycholic acid (9.75 μM), taurocholic acid (TCA) (20.52 μM), glycocholic acid (GCA) (7.466 μM) and lithocholic acid (LCA) (0.413 μM) in PZH after treatment with cholestyramine resin decreased the mRNA levels of TNF-α and IL-1β induced by LPS. (G) Peritoneal macrophages were pretreated with PZH (1.25 mg/mL), cholestyramine resin-treated PZH (1.25 mg/mL), and cholestyramine resin-treated PZH (1.25 mg/mL) + BAs for 2 h and then treated with LPS (100 ng/mL) for 40 min . Replenishing BAs including CA (61.53 μM), DCA (27.25 μM), chenodexycholic acid (9.75 μM), TCA (20.52 μM), GCA (7.466 μM) and LCA (0.413 μM) in PZH after treatment with cholestyramine resin decreased the expression of p-p65 and p-ERK induced by LPS. (H) Schematic model of the mechanism by which PZH attenuates the LPS-induced inflammatory response by activating TGR5-STAT3-A20 signalling pathway. PZH stimulates the phosphorylation of STAT3, which acts as a transcriptional activator for A20 to increase the expression of A20. A20 inhibits the activation of the nuclear factor-kappa B (NF-κB) and mitogen-activated protein kinase (MAPK) signalling pathways to decrease the production of proinflammatory cytokines to attenuate the sepsis progression. The results are representative of one of three experiments. The data are shown as the mean ± standard deviation (SD). ∗∗ P < 0.01, ∗∗∗ P < 0.001, ns: no significance, based on one-way analysis of variance (ANOVA) and two-tailed Student's t -test. CHOL: cholestyramine resin; TRAF6: tumor necrosis factor receptor-associated factor 6; IKK: nuclear factor- kappa B kinase; TAK1: transforming growth factor beta-activated kinase 1; IκBα: nuclear factor-kappa B inhibitor alpha.
Bile Acid Binding Resins Cholestyramine Questran Light, supplied by Bristol Myers, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Bio-Serv cholestyramine (resin
Bile acid (BA), which is an important functional component in Pien Tze Huang (PZH), regulates activation of the G protein-coupled bile acid receptor 1 (TGR5)-signal transducer and activator of transcription 3 (STAT3)-A20 signalling pathway. (A) Total BA levels were detected in the PZH solution and PZH plus <t>cholestyramine</t> resin. (B) Liquid chromatography-mass spectrometry (LC-MS) analysis of PZH supernatant treated with or without cholestyramine resin. (C) Peritoneal macrophages were pretreated with PZH (1.25 mg/mL) or cholestyramine resin-treated PZH (1.25 mg/mL) for 2 h, and then treated with lipopolysaccharide (LPS) (100 ng/mL) for 40 min. PZH treated with cholestyramine resin did not increase the protein expression of TGR5, phospho-STAT3 (p-STAT3) and A20 or decrease the protein expression of phospho-p65 (p-p65), phospho-extracellular signal-regulated kinases (p-ERK), and phosphor-C-Jun N-terminal kinases (p-JNK) induced by LPS. (D) Peritoneal macrophages were pretreated with PZH (1.25 mg/mL) or cholestyramine resin-treated PZH (1.25 mg/mL) for 2 h and then treated with LPS (100 ng/mL) for 6 h. PZH treated with cholestyramine resin did not decrease the mRNA levels of interleukin (IL)-6, tumour necrosis factor-α (TNF-α) and IL-1β induced by LPS. (E) The composition of BAs in the PZH solution was detected by LC-MS. (F) Peritoneal macrophages were pretreated with PZH (1.25 mg/mL), cholestyramine resin-treated PZH (1.25 mg/mL), and cholestyramine resin-treated PZH (1.25 mg/mL) + BAs for 2 h, respectively, and then treated with LPS (100 ng/mL) for 6 h. Replenishing BAs including cholic acid (CA) (61.53 μM), deoxycholic acid (DCA) (27.25 μM), chenodexycholic acid (9.75 μM), taurocholic acid (TCA) (20.52 μM), glycocholic acid (GCA) (7.466 μM) and lithocholic acid (LCA) (0.413 μM) in PZH after treatment with cholestyramine resin decreased the mRNA levels of TNF-α and IL-1β induced by LPS. (G) Peritoneal macrophages were pretreated with PZH (1.25 mg/mL), cholestyramine resin-treated PZH (1.25 mg/mL), and cholestyramine resin-treated PZH (1.25 mg/mL) + BAs for 2 h and then treated with LPS (100 ng/mL) for 40 min . Replenishing BAs including CA (61.53 μM), DCA (27.25 μM), chenodexycholic acid (9.75 μM), TCA (20.52 μM), GCA (7.466 μM) and LCA (0.413 μM) in PZH after treatment with cholestyramine resin decreased the expression of p-p65 and p-ERK induced by LPS. (H) Schematic model of the mechanism by which PZH attenuates the LPS-induced inflammatory response by activating TGR5-STAT3-A20 signalling pathway. PZH stimulates the phosphorylation of STAT3, which acts as a transcriptional activator for A20 to increase the expression of A20. A20 inhibits the activation of the nuclear factor-kappa B (NF-κB) and mitogen-activated protein kinase (MAPK) signalling pathways to decrease the production of proinflammatory cytokines to attenuate the sepsis progression. The results are representative of one of three experiments. The data are shown as the mean ± standard deviation (SD). ∗∗ P < 0.01, ∗∗∗ P < 0.001, ns: no significance, based on one-way analysis of variance (ANOVA) and two-tailed Student's t -test. CHOL: cholestyramine resin; TRAF6: tumor necrosis factor receptor-associated factor 6; IKK: nuclear factor- kappa B kinase; TAK1: transforming growth factor beta-activated kinase 1; IκBα: nuclear factor-kappa B inhibitor alpha.
Cholestyramine (Resin, supplied by Bio-Serv, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Mead Johnson ion-exchange resin cholestyramine questran
Bile acid (BA), which is an important functional component in Pien Tze Huang (PZH), regulates activation of the G protein-coupled bile acid receptor 1 (TGR5)-signal transducer and activator of transcription 3 (STAT3)-A20 signalling pathway. (A) Total BA levels were detected in the PZH solution and PZH plus <t>cholestyramine</t> resin. (B) Liquid chromatography-mass spectrometry (LC-MS) analysis of PZH supernatant treated with or without cholestyramine resin. (C) Peritoneal macrophages were pretreated with PZH (1.25 mg/mL) or cholestyramine resin-treated PZH (1.25 mg/mL) for 2 h, and then treated with lipopolysaccharide (LPS) (100 ng/mL) for 40 min. PZH treated with cholestyramine resin did not increase the protein expression of TGR5, phospho-STAT3 (p-STAT3) and A20 or decrease the protein expression of phospho-p65 (p-p65), phospho-extracellular signal-regulated kinases (p-ERK), and phosphor-C-Jun N-terminal kinases (p-JNK) induced by LPS. (D) Peritoneal macrophages were pretreated with PZH (1.25 mg/mL) or cholestyramine resin-treated PZH (1.25 mg/mL) for 2 h and then treated with LPS (100 ng/mL) for 6 h. PZH treated with cholestyramine resin did not decrease the mRNA levels of interleukin (IL)-6, tumour necrosis factor-α (TNF-α) and IL-1β induced by LPS. (E) The composition of BAs in the PZH solution was detected by LC-MS. (F) Peritoneal macrophages were pretreated with PZH (1.25 mg/mL), cholestyramine resin-treated PZH (1.25 mg/mL), and cholestyramine resin-treated PZH (1.25 mg/mL) + BAs for 2 h, respectively, and then treated with LPS (100 ng/mL) for 6 h. Replenishing BAs including cholic acid (CA) (61.53 μM), deoxycholic acid (DCA) (27.25 μM), chenodexycholic acid (9.75 μM), taurocholic acid (TCA) (20.52 μM), glycocholic acid (GCA) (7.466 μM) and lithocholic acid (LCA) (0.413 μM) in PZH after treatment with cholestyramine resin decreased the mRNA levels of TNF-α and IL-1β induced by LPS. (G) Peritoneal macrophages were pretreated with PZH (1.25 mg/mL), cholestyramine resin-treated PZH (1.25 mg/mL), and cholestyramine resin-treated PZH (1.25 mg/mL) + BAs for 2 h and then treated with LPS (100 ng/mL) for 40 min . Replenishing BAs including CA (61.53 μM), DCA (27.25 μM), chenodexycholic acid (9.75 μM), TCA (20.52 μM), GCA (7.466 μM) and LCA (0.413 μM) in PZH after treatment with cholestyramine resin decreased the expression of p-p65 and p-ERK induced by LPS. (H) Schematic model of the mechanism by which PZH attenuates the LPS-induced inflammatory response by activating TGR5-STAT3-A20 signalling pathway. PZH stimulates the phosphorylation of STAT3, which acts as a transcriptional activator for A20 to increase the expression of A20. A20 inhibits the activation of the nuclear factor-kappa B (NF-κB) and mitogen-activated protein kinase (MAPK) signalling pathways to decrease the production of proinflammatory cytokines to attenuate the sepsis progression. The results are representative of one of three experiments. The data are shown as the mean ± standard deviation (SD). ∗∗ P < 0.01, ∗∗∗ P < 0.001, ns: no significance, based on one-way analysis of variance (ANOVA) and two-tailed Student's t -test. CHOL: cholestyramine resin; TRAF6: tumor necrosis factor receptor-associated factor 6; IKK: nuclear factor- kappa B kinase; TAK1: transforming growth factor beta-activated kinase 1; IκBα: nuclear factor-kappa B inhibitor alpha.
Ion Exchange Resin Cholestyramine Questran, supplied by Mead Johnson, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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MWD promotes colitis development in their progeny by producing DCA. a As shown in Fig. a, WT mice ( n = 5) were colonized with gut microbiota from the W-N and N-N groups. Then, the concentration of DCA in the mice’s feces was measured using an ELISA assay kit. b – g Cholestyramine resin (resin) was given to mice in the W-N and N-N groups ( n = 6 per group) for 5 days to eliminate intestinal bile acids. Following that, mice were given TNBS to induce colitis. c Body weight changes in mice were evaluated daily after TNBS treatment. d Representative images of TNBS-treated colon in N-N+resin and W-N+resin groups. e The mice were sacrificed on day 4, and the colon length was recorded. f , g Histopathological analysis of colon sections. f Histological scores of colitis were assessed. g Representative images of the H&E-stained colon sections of relevant groups (scale bars 100 μm). a , c , e , and f Data represent means ± SEM; NS, not significant; ** P < 0.01; by unpaired Student’s t test. The data shown are representative of three independent experiments

Journal: Microbiome

Article Title: Maternal Western diet mediates susceptibility of offspring to Crohn’s-like colitis by deoxycholate generation

doi: 10.1186/s40168-023-01546-6

Figure Lengend Snippet: MWD promotes colitis development in their progeny by producing DCA. a As shown in Fig. a, WT mice ( n = 5) were colonized with gut microbiota from the W-N and N-N groups. Then, the concentration of DCA in the mice’s feces was measured using an ELISA assay kit. b – g Cholestyramine resin (resin) was given to mice in the W-N and N-N groups ( n = 6 per group) for 5 days to eliminate intestinal bile acids. Following that, mice were given TNBS to induce colitis. c Body weight changes in mice were evaluated daily after TNBS treatment. d Representative images of TNBS-treated colon in N-N+resin and W-N+resin groups. e The mice were sacrificed on day 4, and the colon length was recorded. f , g Histopathological analysis of colon sections. f Histological scores of colitis were assessed. g Representative images of the H&E-stained colon sections of relevant groups (scale bars 100 μm). a , c , e , and f Data represent means ± SEM; NS, not significant; ** P < 0.01; by unpaired Student’s t test. The data shown are representative of three independent experiments

Article Snippet: Cholestyramine resin (11,041–12-6) was obtained from MedChem Express.

Techniques: Concentration Assay, Enzyme-linked Immunosorbent Assay, Staining

FTIR spectra of DFS, Duolite TM AP 143/1083 (IR) and DFS:IR complex.

Journal: Drug Delivery

Article Title: Diclofenac sodium ion exchange resin complex loaded melt cast films for sustained release ocular delivery

doi: 10.1080/10717544.2016.1256000

Figure Lengend Snippet: FTIR spectra of DFS, Duolite TM AP 143/1083 (IR) and DFS:IR complex.

Article Snippet: PEO [PolyOx® WSR N-10 (PEO N-10), MW: 100 000 Da; PubChem CID: 5327147] and Duolite TM AP 143/1083 (Cholestyramine Resin USP; PubChem CID: 70695641) were kindly donated by Dow Chemical Company (Midland, MI).

Techniques:

Mice (129/SvJ) receiving chow containing cholestyramine resin or control chow were pre-treated with streptomycin and infected with an equal mixture of the S. Typhimurium wild type and a fepE mutant. (A) Competitive indices recovered from feces over time. (B) Competitive indices recovered from colon contents. (C) Determination of concentrations of total bile acids in colon contents. (A–C) Bars represent geometric means ± standard error. *, P <0.05; **, P <0.01. (D) Combined histopathology score of pathological changes observed in sections from the cecum. Lines represent averages. Each circle or diamond represents the combined histopathology score from an individual animal. (E) Representative images of histopathological changes.

Journal: PLoS Pathogens

Article Title: Very Long O-antigen Chains Enhance Fitness during Salmonella -induced Colitis by Increasing Bile Resistance

doi: 10.1371/journal.ppat.1002918

Figure Lengend Snippet: Mice (129/SvJ) receiving chow containing cholestyramine resin or control chow were pre-treated with streptomycin and infected with an equal mixture of the S. Typhimurium wild type and a fepE mutant. (A) Competitive indices recovered from feces over time. (B) Competitive indices recovered from colon contents. (C) Determination of concentrations of total bile acids in colon contents. (A–C) Bars represent geometric means ± standard error. *, P <0.05; **, P <0.01. (D) Combined histopathology score of pathological changes observed in sections from the cecum. Lines represent averages. Each circle or diamond represents the combined histopathology score from an individual animal. (E) Representative images of histopathological changes.

Article Snippet: In some experiments, 129/SvJ mice were fed a normal rodent diet (Harlan-Teklad) supplemented with the bile acid sequestrant cholestyramine resin (2%, The Dow Chemical Company) starting the day before streptomycin treatment and continuing throughout the experiment.

Techniques: Control, Infection, Mutagenesis, Histopathology

Classification of drugs

Journal: Annals of Dermatology

Article Title: The Risk of Rosacea According to Chronic Diseases and Medications: A 5-Year Retrospective, Multi-Institutional Case-Control Study

doi: 10.5021/ad.2018.30.6.676

Figure Lengend Snippet: Classification of drugs

Article Snippet: Cholestyramine , , Cholestyramine Resin 4 g/9 g (Questran Powder for Suspension Boryung Boryung Pharm, Seoul, Korea).

Techniques: Suspension

The risk of diagnosed rosacea according to chronic systemic diseases, which is related to cardiovascular risk factors, and drugs

Journal: Annals of Dermatology

Article Title: The Risk of Rosacea According to Chronic Diseases and Medications: A 5-Year Retrospective, Multi-Institutional Case-Control Study

doi: 10.5021/ad.2018.30.6.676

Figure Lengend Snippet: The risk of diagnosed rosacea according to chronic systemic diseases, which is related to cardiovascular risk factors, and drugs

Article Snippet: Cholestyramine , , Cholestyramine Resin 4 g/9 g (Questran Powder for Suspension Boryung Boryung Pharm, Seoul, Korea).

Techniques:

Bile acid (BA), which is an important functional component in Pien Tze Huang (PZH), regulates activation of the G protein-coupled bile acid receptor 1 (TGR5)-signal transducer and activator of transcription 3 (STAT3)-A20 signalling pathway. (A) Total BA levels were detected in the PZH solution and PZH plus cholestyramine resin. (B) Liquid chromatography-mass spectrometry (LC-MS) analysis of PZH supernatant treated with or without cholestyramine resin. (C) Peritoneal macrophages were pretreated with PZH (1.25 mg/mL) or cholestyramine resin-treated PZH (1.25 mg/mL) for 2 h, and then treated with lipopolysaccharide (LPS) (100 ng/mL) for 40 min. PZH treated with cholestyramine resin did not increase the protein expression of TGR5, phospho-STAT3 (p-STAT3) and A20 or decrease the protein expression of phospho-p65 (p-p65), phospho-extracellular signal-regulated kinases (p-ERK), and phosphor-C-Jun N-terminal kinases (p-JNK) induced by LPS. (D) Peritoneal macrophages were pretreated with PZH (1.25 mg/mL) or cholestyramine resin-treated PZH (1.25 mg/mL) for 2 h and then treated with LPS (100 ng/mL) for 6 h. PZH treated with cholestyramine resin did not decrease the mRNA levels of interleukin (IL)-6, tumour necrosis factor-α (TNF-α) and IL-1β induced by LPS. (E) The composition of BAs in the PZH solution was detected by LC-MS. (F) Peritoneal macrophages were pretreated with PZH (1.25 mg/mL), cholestyramine resin-treated PZH (1.25 mg/mL), and cholestyramine resin-treated PZH (1.25 mg/mL) + BAs for 2 h, respectively, and then treated with LPS (100 ng/mL) for 6 h. Replenishing BAs including cholic acid (CA) (61.53 μM), deoxycholic acid (DCA) (27.25 μM), chenodexycholic acid (9.75 μM), taurocholic acid (TCA) (20.52 μM), glycocholic acid (GCA) (7.466 μM) and lithocholic acid (LCA) (0.413 μM) in PZH after treatment with cholestyramine resin decreased the mRNA levels of TNF-α and IL-1β induced by LPS. (G) Peritoneal macrophages were pretreated with PZH (1.25 mg/mL), cholestyramine resin-treated PZH (1.25 mg/mL), and cholestyramine resin-treated PZH (1.25 mg/mL) + BAs for 2 h and then treated with LPS (100 ng/mL) for 40 min . Replenishing BAs including CA (61.53 μM), DCA (27.25 μM), chenodexycholic acid (9.75 μM), TCA (20.52 μM), GCA (7.466 μM) and LCA (0.413 μM) in PZH after treatment with cholestyramine resin decreased the expression of p-p65 and p-ERK induced by LPS. (H) Schematic model of the mechanism by which PZH attenuates the LPS-induced inflammatory response by activating TGR5-STAT3-A20 signalling pathway. PZH stimulates the phosphorylation of STAT3, which acts as a transcriptional activator for A20 to increase the expression of A20. A20 inhibits the activation of the nuclear factor-kappa B (NF-κB) and mitogen-activated protein kinase (MAPK) signalling pathways to decrease the production of proinflammatory cytokines to attenuate the sepsis progression. The results are representative of one of three experiments. The data are shown as the mean ± standard deviation (SD). ∗∗ P < 0.01, ∗∗∗ P < 0.001, ns: no significance, based on one-way analysis of variance (ANOVA) and two-tailed Student's t -test. CHOL: cholestyramine resin; TRAF6: tumor necrosis factor receptor-associated factor 6; IKK: nuclear factor- kappa B kinase; TAK1: transforming growth factor beta-activated kinase 1; IκBα: nuclear factor-kappa B inhibitor alpha.

Journal: Journal of Pharmaceutical Analysis

Article Title: Traditional Chinese medicine Pien-Tze-Huang ameliorates LPS-induced sepsis through bile acid-mediated activation of TGR5-STAT3-A20 signalling

doi: 10.1016/j.jpha.2023.12.005

Figure Lengend Snippet: Bile acid (BA), which is an important functional component in Pien Tze Huang (PZH), regulates activation of the G protein-coupled bile acid receptor 1 (TGR5)-signal transducer and activator of transcription 3 (STAT3)-A20 signalling pathway. (A) Total BA levels were detected in the PZH solution and PZH plus cholestyramine resin. (B) Liquid chromatography-mass spectrometry (LC-MS) analysis of PZH supernatant treated with or without cholestyramine resin. (C) Peritoneal macrophages were pretreated with PZH (1.25 mg/mL) or cholestyramine resin-treated PZH (1.25 mg/mL) for 2 h, and then treated with lipopolysaccharide (LPS) (100 ng/mL) for 40 min. PZH treated with cholestyramine resin did not increase the protein expression of TGR5, phospho-STAT3 (p-STAT3) and A20 or decrease the protein expression of phospho-p65 (p-p65), phospho-extracellular signal-regulated kinases (p-ERK), and phosphor-C-Jun N-terminal kinases (p-JNK) induced by LPS. (D) Peritoneal macrophages were pretreated with PZH (1.25 mg/mL) or cholestyramine resin-treated PZH (1.25 mg/mL) for 2 h and then treated with LPS (100 ng/mL) for 6 h. PZH treated with cholestyramine resin did not decrease the mRNA levels of interleukin (IL)-6, tumour necrosis factor-α (TNF-α) and IL-1β induced by LPS. (E) The composition of BAs in the PZH solution was detected by LC-MS. (F) Peritoneal macrophages were pretreated with PZH (1.25 mg/mL), cholestyramine resin-treated PZH (1.25 mg/mL), and cholestyramine resin-treated PZH (1.25 mg/mL) + BAs for 2 h, respectively, and then treated with LPS (100 ng/mL) for 6 h. Replenishing BAs including cholic acid (CA) (61.53 μM), deoxycholic acid (DCA) (27.25 μM), chenodexycholic acid (9.75 μM), taurocholic acid (TCA) (20.52 μM), glycocholic acid (GCA) (7.466 μM) and lithocholic acid (LCA) (0.413 μM) in PZH after treatment with cholestyramine resin decreased the mRNA levels of TNF-α and IL-1β induced by LPS. (G) Peritoneal macrophages were pretreated with PZH (1.25 mg/mL), cholestyramine resin-treated PZH (1.25 mg/mL), and cholestyramine resin-treated PZH (1.25 mg/mL) + BAs for 2 h and then treated with LPS (100 ng/mL) for 40 min . Replenishing BAs including CA (61.53 μM), DCA (27.25 μM), chenodexycholic acid (9.75 μM), TCA (20.52 μM), GCA (7.466 μM) and LCA (0.413 μM) in PZH after treatment with cholestyramine resin decreased the expression of p-p65 and p-ERK induced by LPS. (H) Schematic model of the mechanism by which PZH attenuates the LPS-induced inflammatory response by activating TGR5-STAT3-A20 signalling pathway. PZH stimulates the phosphorylation of STAT3, which acts as a transcriptional activator for A20 to increase the expression of A20. A20 inhibits the activation of the nuclear factor-kappa B (NF-κB) and mitogen-activated protein kinase (MAPK) signalling pathways to decrease the production of proinflammatory cytokines to attenuate the sepsis progression. The results are representative of one of three experiments. The data are shown as the mean ± standard deviation (SD). ∗∗ P < 0.01, ∗∗∗ P < 0.001, ns: no significance, based on one-way analysis of variance (ANOVA) and two-tailed Student's t -test. CHOL: cholestyramine resin; TRAF6: tumor necrosis factor receptor-associated factor 6; IKK: nuclear factor- kappa B kinase; TAK1: transforming growth factor beta-activated kinase 1; IκBα: nuclear factor-kappa B inhibitor alpha.

Article Snippet: Cholestyramine resin was purchased from Shanghai Yuanye Bio-Technology Co., Ltd (Shanghai, China).

Techniques: Functional Assay, Activation Assay, Liquid Chromatography, Mass Spectrometry, Liquid Chromatography with Mass Spectroscopy, Expressing, Phospho-proteomics, Standard Deviation, Two Tailed Test