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steraloids inc glycochenodeoxycholic acid gcdca
Glycochenodeoxycholic Acid Gcdca, supplied by steraloids inc, used in various techniques. Bioz Stars score: 93/100, based on 13 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/glycochenodeoxycholic+acid/5%CE%B2-CHOLANIC+ACID-3%CE%B1%2C+7%CE%B1-DIOL+N-(CARBOXYMETHYL)-AMIDE/pmc12838154-53-25-52
Average 93 stars, based on 13 article reviews

glycochenodeoxycholic acid gcdca - by Bioz Stars, 2026-10

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Article Title: Cross-Validation of Metabolic Phenotypes in SARS-CoV-2 Infected Subpopulations Using Targeted Liquid Chromatography-Mass Spectrometry (LC-MS).
Article Snippet: .. Bile acid data were collected using an in-house protocol developed and validated following fit-for-purpose recommendations for bioanalytical workflows from the European Bioanalysis Forum adapted from the US Food and Drug administration.21,22 Bile acid standards: chenodeoxycholic acid, cholic acid, glycochenodeoxycholic acid, glycocholic acid, glycodeoxycholic acid, glycoursodeoxycholic acid, taurocholic acid, taurochenodeoxycholic acid, taurodeoxycholic acid, ursodeoxycholic acid, deoxycholic acid, glycolithocholic acid, lithocholic acid, taurohyodeoxycholic acid, and taurolithocholic acid were purchased from Steraloids (Newport, RI, USA). .. Stable isotope labeled internal standard mixtures of unconjugated and conjugated bile acids were purchased from Cambridge Isotope Laboratories (Tewksbury, MA, USA) (Table S1).

High Content Screening:

Article Title: Elevated Levels of Toxic Bile Acids in Serum of Cystic Fibrosis Patients with CFTR Mutations Causing Pancreatic Insufficiency.
Article Snippet: OASISTM3cc HLB cartridges were obtained from Waters Corporation Milford, MA, USA. .. The following free and conjugated BAs were purchased from Steraloids (Wilton, NH, USA): cholic acid (CA), glycocholic acid (G-CA), taurocholic acid (T-CA), chenodeoxycholic acid (CDCA), glycochenodeoxycholic acid (G-CDCA), taurochenodeoxycholic acid (TCDCA), deoxycholic acid (DCA), glycodeoxycholic acid (G-DCA), taurodeoxycholic acid (TDCA), lithocholic acid (LCA), glycolithocholic acid (G-LCA), taurolithocholic acid (T-LCA), hyodeoxycholic acid (HDCA), glycohyodeoxycholic acid (G-HDCA), taurohyodeoxycholic acid (T-HDCA), hyocholic acid (HCA), glycohyocholic acid (G-HCA), taurohyocholic acid (T-HCA), α-murocholic acid (α-MCA), β-muricholic acid (β-MCA), murocholic acid (MOCA), and tauro-β-muricholic acid (T-β-MCA). ..

Article Title: Elevated Levels of Toxic Bile Acids in Serum of Cystic Fibrosis Patients with CFTR Mutations Causing Pancreatic Insufficiency
Article Snippet: OASISTM3cc HLB cartridges were obtained from Waters Corporation Milford, MA, USA. .. The following free and conjugated BAs were purchased from Steraloids (Wilton, NH, USA): cholic acid (CA), glycocholic acid (G-CA), taurocholic acid (T-CA), chenodeoxycholic acid (CDCA), glycochenodeoxycholic acid (G-CDCA), taurochenodeoxycholic acid (T-CDCA), deoxycholic acid (DCA), glycodeoxycholic acid (G-DCA), taurodeoxycholic acid (T-DCA), lithocholic acid (LCA), glycolithocholic acid (G-LCA), taurolithocholic acid (T-LCA), hyodeoxycholic acid (HDCA), glycohyodeoxycholic acid (G-HDCA), taurohyodeoxycholic acid (T-HDCA), hyocholic acid (HCA), glycohyocholic acid (G-HCA), taurohyocholic acid (T-HCA), α-murocholic acid (α-MCA), β-muricholic acid (β-MCA), murocholic acid (MOCA), and tauro-β-muricholic acid (T-β-MCA). ..

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GCDCA promotes the HCC progression and increases hepatocellular carcinoma cell stemness. (A) Flow chart of animal experiments. (B) Kaplan–Meier plots of DEN-induced primary hepatocellular carcinoma in rats after administration of GCDCA and cholestyramine ( n = 5 in each group). (C) Representative images of liver tumors in different groups of rats (scale bar = 1 cm) and HE-stained images (scale bar = 200 μm). (D, E) Maximum diameters of liver tumors in rats in different groups and the number of tumors for quantitative analysis ( n = 5 in each group). (F, H) Serum AST and ALT activities and TBA levels in different groups of rats ( n = 4 in each group). (I) Representative immunohistochemical staining of KRT19-, EPCAM-, and SOX9-positive cells in the livers of different groups of rats, scale bar = 100 μm ( n = 3 in each group). (J) Representative immunofluorescence staining of co-localized positive cells of KRT19 (red), EPCAM (green), and SOX9 (pink) in liver CSCs of different groups of rats. Cell nuclei were stained with DAPI (blue). Scale bar = 50 μm. * p < 0.05, ** p < 0.01, and *** p < 0.001, n.s., not significant.

Journal: Frontiers in Immunology

Article Title: GCDCA promotes hepatocellular carcinoma progression through S1PR2/PI3K/AKT-mediated polarization of M2-type macrophages

doi: 10.3389/fimmu.2026.1640450

Figure Lengend Snippet: GCDCA promotes the HCC progression and increases hepatocellular carcinoma cell stemness. (A) Flow chart of animal experiments. (B) Kaplan–Meier plots of DEN-induced primary hepatocellular carcinoma in rats after administration of GCDCA and cholestyramine ( n = 5 in each group). (C) Representative images of liver tumors in different groups of rats (scale bar = 1 cm) and HE-stained images (scale bar = 200 μm). (D, E) Maximum diameters of liver tumors in rats in different groups and the number of tumors for quantitative analysis ( n = 5 in each group). (F, H) Serum AST and ALT activities and TBA levels in different groups of rats ( n = 4 in each group). (I) Representative immunohistochemical staining of KRT19-, EPCAM-, and SOX9-positive cells in the livers of different groups of rats, scale bar = 100 μm ( n = 3 in each group). (J) Representative immunofluorescence staining of co-localized positive cells of KRT19 (red), EPCAM (green), and SOX9 (pink) in liver CSCs of different groups of rats. Cell nuclei were stained with DAPI (blue). Scale bar = 50 μm. * p < 0.05, ** p < 0.01, and *** p < 0.001, n.s., not significant.

Article Snippet: JTE-013 was injected intraperitoneally 2 h before GCDCA administration at a dose of 2 mg/kg body weight in the JTE-013 (TargetMol, China) interference model, starting at week 12 of DEN treatment.

Techniques: Staining, Immunohistochemical staining, Immunofluorescence

GCDCA does not directly promote stemness in hepatocellular carcinoma cells. (A) Relative viability values of hepatocellular carcinoma cells in different concentrations of GCDCA ( n = 3 in each group). (B) Effect of GCDCA on clonogenic ability of different hepatocellular carcinoma cell lines. (C) Effect of GCDCA on sphere-forming ability of different hepatocellular carcinoma cell lines. Scale bar = 50 µm. Cell clones were counted using ImageJ 1.43. * p < 0.05, ** p < 0.01, and *** p < 0.001, n.s., not significant.

Journal: Frontiers in Immunology

Article Title: GCDCA promotes hepatocellular carcinoma progression through S1PR2/PI3K/AKT-mediated polarization of M2-type macrophages

doi: 10.3389/fimmu.2026.1640450

Figure Lengend Snippet: GCDCA does not directly promote stemness in hepatocellular carcinoma cells. (A) Relative viability values of hepatocellular carcinoma cells in different concentrations of GCDCA ( n = 3 in each group). (B) Effect of GCDCA on clonogenic ability of different hepatocellular carcinoma cell lines. (C) Effect of GCDCA on sphere-forming ability of different hepatocellular carcinoma cell lines. Scale bar = 50 µm. Cell clones were counted using ImageJ 1.43. * p < 0.05, ** p < 0.01, and *** p < 0.001, n.s., not significant.

Techniques: Clone Assay

GCDCA-induced polarization of M2 macrophages promotes stemness in hepatocellular carcinoma cells. (A) Expression of M2 macrophage marker genes Mrc1 , Cd163 , Arg1 in NR8383 cells after GCDCA treatment (n = 3 in each group). (B) Expression of CD206, CD163, ARG1 proteins in NR8383 cells. (C) Expression of M2 macrophage marker genes MRC1 , ARG1 , and TGF-β in THP-1 cells after GCDCA treatment (n = 3 in each group). (D) Expression of CD206, CD163, ARG1 proteins in THP-1 cells. (E) Co-culture pattern of NR8383 and RH35 cells. (F) Expression of stemness genes Krt19 , Epcam , and Sox9 in RH35 cells after co-culture with GCDCA-treated NR8383 cells (n =3 in each group). (G) Expression of KRT19, EPCAM, and SOX9 proteins in RH35 cells. (H) Co-culture pattern of THP-1 and Huh7. (I) Expression of stemness genes KRT19 , EPCAM , and SOX9 in Huh7 cells after co-culture with GCDCA-treated THP-1 cells (n = 3 in each group). (J) Expression of KRT19, EPCAM, and SOX9 proteins in Huh7 cells. GAPDH was used as an internal reference. * p < 0.05, ** p < 0.01, and *** p < 0.001, n.s., not significant.

Journal: Frontiers in Immunology

Article Title: GCDCA promotes hepatocellular carcinoma progression through S1PR2/PI3K/AKT-mediated polarization of M2-type macrophages

doi: 10.3389/fimmu.2026.1640450

Figure Lengend Snippet: GCDCA-induced polarization of M2 macrophages promotes stemness in hepatocellular carcinoma cells. (A) Expression of M2 macrophage marker genes Mrc1 , Cd163 , Arg1 in NR8383 cells after GCDCA treatment (n = 3 in each group). (B) Expression of CD206, CD163, ARG1 proteins in NR8383 cells. (C) Expression of M2 macrophage marker genes MRC1 , ARG1 , and TGF-β in THP-1 cells after GCDCA treatment (n = 3 in each group). (D) Expression of CD206, CD163, ARG1 proteins in THP-1 cells. (E) Co-culture pattern of NR8383 and RH35 cells. (F) Expression of stemness genes Krt19 , Epcam , and Sox9 in RH35 cells after co-culture with GCDCA-treated NR8383 cells (n =3 in each group). (G) Expression of KRT19, EPCAM, and SOX9 proteins in RH35 cells. (H) Co-culture pattern of THP-1 and Huh7. (I) Expression of stemness genes KRT19 , EPCAM , and SOX9 in Huh7 cells after co-culture with GCDCA-treated THP-1 cells (n = 3 in each group). (J) Expression of KRT19, EPCAM, and SOX9 proteins in Huh7 cells. GAPDH was used as an internal reference. * p < 0.05, ** p < 0.01, and *** p < 0.001, n.s., not significant.

Techniques: Expressing, Marker, Co-Culture Assay

GCDCA induces M2-type polarization in macrophages through activation of S1PR2 receptors. (A) Single-cell sequencing to analyze bile acid receptor expression in M2 macrophages. (B) Activation of the S1PR2 receptor by GCDCA was detected using the Tango GPCR assay (n = 3 in each group). (C, D) TCGA database analysis of S1PR2 correlation with KRT19 , EPCAM , SOX9 , CD68 , MRC1 , CD163 . (E) Representative immunohistochemical staining of CD68, CD163, and S1PR2-positive cells in the livers of different groups of rats, scale bar = 100 μm (n = 3 in each group). (F) Representative immunofluorescence staining of S1PR2 (red) co-localized with CD163- (green) and CD206-(green) positive cells in the livers of different groups of rats, scale bar = 100 μm. * p < 0.05, ** p < 0.01, and *** p < 0.001, n.s., not significant.

Journal: Frontiers in Immunology

Article Title: GCDCA promotes hepatocellular carcinoma progression through S1PR2/PI3K/AKT-mediated polarization of M2-type macrophages

doi: 10.3389/fimmu.2026.1640450

Figure Lengend Snippet: GCDCA induces M2-type polarization in macrophages through activation of S1PR2 receptors. (A) Single-cell sequencing to analyze bile acid receptor expression in M2 macrophages. (B) Activation of the S1PR2 receptor by GCDCA was detected using the Tango GPCR assay (n = 3 in each group). (C, D) TCGA database analysis of S1PR2 correlation with KRT19 , EPCAM , SOX9 , CD68 , MRC1 , CD163 . (E) Representative immunohistochemical staining of CD68, CD163, and S1PR2-positive cells in the livers of different groups of rats, scale bar = 100 μm (n = 3 in each group). (F) Representative immunofluorescence staining of S1PR2 (red) co-localized with CD163- (green) and CD206-(green) positive cells in the livers of different groups of rats, scale bar = 100 μm. * p < 0.05, ** p < 0.01, and *** p < 0.001, n.s., not significant.

Techniques: Activation Assay, Single Cell, Sequencing, Expressing, Immunohistochemical staining, Staining, Immunofluorescence

Pharmacological inhibition of S1PR2 by JTE-013 reverses GCDCA-induced stemness. (A) Flow chart of animal experiments. (B) Kaplan–Meier plots of DEN-induced primary hepatocellular carcinoma in rats after administration of GCDCA and the receptor inhibitor JTE-013 ( n = 5 in each group). (C) Representative images of liver tumors in different groups of rats (scale bar = 1 cm) and HE-stained images (scale bar = 200 μm). (D, E) Analysis of maximum diameter and number of tumors (n = 4 in each group). (F–H) Serum AST and ALT activities and TBA levels in different groups of rats (n = 4 in each group). (I) Representative immunohistochemical staining of KRT19, EPCAM, and SOX9-positive cells in the livers of different groups of rats, scale bar = 200 μm (n = 3 in each group). (J) Representative immunofluorescence staining of KRT19, EPCAM, and SOX9 co-localized positive cells in the livers of different groups of rats, scale bar = 50 μm. * p < 0.05, ** p < 0.01, and *** p < 0.001, n.s., not significant.

Journal: Frontiers in Immunology

Article Title: GCDCA promotes hepatocellular carcinoma progression through S1PR2/PI3K/AKT-mediated polarization of M2-type macrophages

doi: 10.3389/fimmu.2026.1640450

Figure Lengend Snippet: Pharmacological inhibition of S1PR2 by JTE-013 reverses GCDCA-induced stemness. (A) Flow chart of animal experiments. (B) Kaplan–Meier plots of DEN-induced primary hepatocellular carcinoma in rats after administration of GCDCA and the receptor inhibitor JTE-013 ( n = 5 in each group). (C) Representative images of liver tumors in different groups of rats (scale bar = 1 cm) and HE-stained images (scale bar = 200 μm). (D, E) Analysis of maximum diameter and number of tumors (n = 4 in each group). (F–H) Serum AST and ALT activities and TBA levels in different groups of rats (n = 4 in each group). (I) Representative immunohistochemical staining of KRT19, EPCAM, and SOX9-positive cells in the livers of different groups of rats, scale bar = 200 μm (n = 3 in each group). (J) Representative immunofluorescence staining of KRT19, EPCAM, and SOX9 co-localized positive cells in the livers of different groups of rats, scale bar = 50 μm. * p < 0.05, ** p < 0.01, and *** p < 0.001, n.s., not significant.

Techniques: Inhibition, Staining, Immunohistochemical staining, Immunofluorescence

Inhibition of S1PR2 receptor reverses GCDCA-induced polarization of M2 macrophages. (A) Expression of M2 macrophage marker genes Mrc1 , Cd163 , and Arg1 in NR8383 cells after inhibition of the S1PR2 receptor (n = 3 in each group). (B) Expression of CD206, CD163, and ARG1 proteins in NR8383 cells after inhibition of the S1PR2 receptor. (C) Expression of M2 macrophage marker genes MRC1 , ARG1 , and TGF-β in THP-1 cells after inhibition of the S1PR2 receptor (n = 3 in each group). (D) Expression of CD206, CD163, and ARG1 proteins in THP-1 cells after inhibition of the S1PR2 receptor. (E) Expression of stemness genes Krt19 , Epcam , and Sox9 in RH35 cells after co-culture with GCDCA-induced NR8383 cells pretreated with JTE-013 (n = 3 in each group). (F) Expression of KRT19, EPCAM, and SOX9 proteins in RH35 cells after co-culture with GCDCA-induced NR8383 cells pretreated with JTE-013. (G) Expression of stemness genes KRT19 , EPCAM , and SOX9 in Huh7 cells after co-culture with GCDCA-induced THP-1 cells pretreated with JTE-013 (n = 3 in each group). (H) Expression of KRT19, EPCAM, and SOX9 proteins in Huh7 cells after co-culture with GCDCA-induced THP-1 cells pretreated with JTE-013. (I-J) Representative immunofluorescence staining of M2 macrophage markers CD206 (white) and CD163 (white) co-localized with KRT19- (red) and EPCAM- (green) positive cells in the livers of different groups of rats, scale bar = 100 μm. GAPDH is used as an internal reference. * p < 0.05, ** p < 0.01, and *** p < 0.001, n.s., not significant.

Journal: Frontiers in Immunology

Article Title: GCDCA promotes hepatocellular carcinoma progression through S1PR2/PI3K/AKT-mediated polarization of M2-type macrophages

doi: 10.3389/fimmu.2026.1640450

Figure Lengend Snippet: Inhibition of S1PR2 receptor reverses GCDCA-induced polarization of M2 macrophages. (A) Expression of M2 macrophage marker genes Mrc1 , Cd163 , and Arg1 in NR8383 cells after inhibition of the S1PR2 receptor (n = 3 in each group). (B) Expression of CD206, CD163, and ARG1 proteins in NR8383 cells after inhibition of the S1PR2 receptor. (C) Expression of M2 macrophage marker genes MRC1 , ARG1 , and TGF-β in THP-1 cells after inhibition of the S1PR2 receptor (n = 3 in each group). (D) Expression of CD206, CD163, and ARG1 proteins in THP-1 cells after inhibition of the S1PR2 receptor. (E) Expression of stemness genes Krt19 , Epcam , and Sox9 in RH35 cells after co-culture with GCDCA-induced NR8383 cells pretreated with JTE-013 (n = 3 in each group). (F) Expression of KRT19, EPCAM, and SOX9 proteins in RH35 cells after co-culture with GCDCA-induced NR8383 cells pretreated with JTE-013. (G) Expression of stemness genes KRT19 , EPCAM , and SOX9 in Huh7 cells after co-culture with GCDCA-induced THP-1 cells pretreated with JTE-013 (n = 3 in each group). (H) Expression of KRT19, EPCAM, and SOX9 proteins in Huh7 cells after co-culture with GCDCA-induced THP-1 cells pretreated with JTE-013. (I-J) Representative immunofluorescence staining of M2 macrophage markers CD206 (white) and CD163 (white) co-localized with KRT19- (red) and EPCAM- (green) positive cells in the livers of different groups of rats, scale bar = 100 μm. GAPDH is used as an internal reference. * p < 0.05, ** p < 0.01, and *** p < 0.001, n.s., not significant.

Techniques: Inhibition, Expressing, Marker, Co-Culture Assay, Immunofluorescence, Staining

GCDCA induces macrophage polarization toward M2 via the S1PR2/PI3K/AKT signaling pathway. (A) Volcano plot of differentially expressed genes (DEGs) between GCDCA-treated and control groups (n = 3 in each group). (B) Histogram of KEGG enrichment results of DEGs between GCDCA-treated and control groups. (C) Bubble plots of GO enrichment results of DEGs between GCDCA-treated and control groups. (D) Western blotting for p-AKT, AKT, p-PI3K, and PI3K protein expression in GCDCA-treated NR8383 cells. (E) Western blotting was used to detect the expression of p-AKT, AKT, p-PI3K, PI3K, CD206, and ARG1 proteins after pretreatment with LY294002 inhibitor.

Journal: Frontiers in Immunology

Article Title: GCDCA promotes hepatocellular carcinoma progression through S1PR2/PI3K/AKT-mediated polarization of M2-type macrophages

doi: 10.3389/fimmu.2026.1640450

Figure Lengend Snippet: GCDCA induces macrophage polarization toward M2 via the S1PR2/PI3K/AKT signaling pathway. (A) Volcano plot of differentially expressed genes (DEGs) between GCDCA-treated and control groups (n = 3 in each group). (B) Histogram of KEGG enrichment results of DEGs between GCDCA-treated and control groups. (C) Bubble plots of GO enrichment results of DEGs between GCDCA-treated and control groups. (D) Western blotting for p-AKT, AKT, p-PI3K, and PI3K protein expression in GCDCA-treated NR8383 cells. (E) Western blotting was used to detect the expression of p-AKT, AKT, p-PI3K, PI3K, CD206, and ARG1 proteins after pretreatment with LY294002 inhibitor.

Techniques: Control, Western Blot, Expressing

GCDCA activates the NLRP3 inflammasome in hepatocytes. ( A ) Dose-dependent effects of GCDCA (25–400 μM, 24 h) on protein levels effects of NLRP3, ASC, pro-caspase-1, caspase-1 P20, pro-IL-1β and GAPDH. ( B ) Time-dependent effects of these proteins in L02 cells treated with 200 μM GCDCA. ( C and D ) Synergistic priming by LPS (1 μg/mL, 4 h pre-treatment): GCDCA (50–400 μM, 24 h) ( C ) or time-dependent (12–72 h) ( D ) enhancement of NLRP3, pro-caspase-1, and pro-IL-1β expression in LPS-primed cells. ( E ) Comparative analysis of NLRP3 inflammasome activationin L02 cells treated with GCDCA (200 μM, 24 h) with/without LPS co-stimulation. ( F ) Essential role of NLRP3 in GCDCA-induced pyroptosis. L02 cells were pretreated with/without LPS (1 μg/mL, 4 h) and MCC950 (10 μM, 2 h) prior to GCDCA (200 μM, 24 h) exposure. Whole cell lysates were examined by Western Blot analysis. Molecular weight markers (kDa) are indicated. n ≥ 3 for each group. (LG200: LPS+200 μM GCDCA; G200: GCDCA 200 μM).

Journal: Journal of Inflammation Research

Article Title: Glycochenodeoxycholic acid induces the release of IL-1beta from L02 cells via the NLRP3/caspase-1/GSDMD pathway to activate LX2 cells

doi: 10.2147/JIR.S532042

Figure Lengend Snippet: GCDCA activates the NLRP3 inflammasome in hepatocytes. ( A ) Dose-dependent effects of GCDCA (25–400 μM, 24 h) on protein levels effects of NLRP3, ASC, pro-caspase-1, caspase-1 P20, pro-IL-1β and GAPDH. ( B ) Time-dependent effects of these proteins in L02 cells treated with 200 μM GCDCA. ( C and D ) Synergistic priming by LPS (1 μg/mL, 4 h pre-treatment): GCDCA (50–400 μM, 24 h) ( C ) or time-dependent (12–72 h) ( D ) enhancement of NLRP3, pro-caspase-1, and pro-IL-1β expression in LPS-primed cells. ( E ) Comparative analysis of NLRP3 inflammasome activationin L02 cells treated with GCDCA (200 μM, 24 h) with/without LPS co-stimulation. ( F ) Essential role of NLRP3 in GCDCA-induced pyroptosis. L02 cells were pretreated with/without LPS (1 μg/mL, 4 h) and MCC950 (10 μM, 2 h) prior to GCDCA (200 μM, 24 h) exposure. Whole cell lysates were examined by Western Blot analysis. Molecular weight markers (kDa) are indicated. n ≥ 3 for each group. (LG200: LPS+200 μM GCDCA; G200: GCDCA 200 μM).

Article Snippet: L02 and LX2 cells were synchronized in serum-free medium for 12 h. L02 cells were exposed to graded GCDCA concentrations (25–400 μM, HY-N2334, MCE) for 24 h or 200 μM GCDCA for 6–72 h to establish dose/time-response profiles.

Techniques: Expressing, Western Blot, Molecular Weight

GCDCA induces GSDMD-mediated pyroptosis in hepatocytes. ( A and B ) Time- and dose-dependent LDH release in LPS-primed L02 cells treated with GCDCA: ( A ) Dose-response (50–400 μM GCDCA, 24 h); ( B ) Time-course (200 μM GCDCA, 12–72 h). ( C ) Dose-dependent GSDMD proteolysis in LPS-primed cells treated with GCDCA (50–400 μM, 24 h); ( D ) Time-dependent GSDMD proteolysis (200 μM GCDCA, 12–72 h). GAPDH serves as loading control. ( E ) Validation of GSDMD knockdown efficiency in L02 cells. ( F ) LDH release in lentiviruses-transfected L02 cells treated with GCDCA (200 μM, 24 h). ( G ) Representative flow plots showing Annexin V/PI staining in lentiviruses-transfected L02 cells. ( H ) Flow cytometry quantification of pyroptotic cells (Annexin V⁺/PI⁺). n ≥ 3 for each group. a P < 0.005, b P < 0.05, c P < 0.0001.

Journal: Journal of Inflammation Research

Article Title: Glycochenodeoxycholic acid induces the release of IL-1beta from L02 cells via the NLRP3/caspase-1/GSDMD pathway to activate LX2 cells

doi: 10.2147/JIR.S532042

Figure Lengend Snippet: GCDCA induces GSDMD-mediated pyroptosis in hepatocytes. ( A and B ) Time- and dose-dependent LDH release in LPS-primed L02 cells treated with GCDCA: ( A ) Dose-response (50–400 μM GCDCA, 24 h); ( B ) Time-course (200 μM GCDCA, 12–72 h). ( C ) Dose-dependent GSDMD proteolysis in LPS-primed cells treated with GCDCA (50–400 μM, 24 h); ( D ) Time-dependent GSDMD proteolysis (200 μM GCDCA, 12–72 h). GAPDH serves as loading control. ( E ) Validation of GSDMD knockdown efficiency in L02 cells. ( F ) LDH release in lentiviruses-transfected L02 cells treated with GCDCA (200 μM, 24 h). ( G ) Representative flow plots showing Annexin V/PI staining in lentiviruses-transfected L02 cells. ( H ) Flow cytometry quantification of pyroptotic cells (Annexin V⁺/PI⁺). n ≥ 3 for each group. a P < 0.005, b P < 0.05, c P < 0.0001.

Techniques: Control, Biomarker Discovery, Knockdown, Transfection, Staining, Flow Cytometry

GCDCA triggers caspase-1-dependent pyroptosis in hepatocytes. ( A and B ) Caspase-1/4 activity in LPS-primed L02 cells treated with GCDCA. ( C and D ) Flow cytometry quantification of pyroptotic cells (Annexin V⁺/PI⁺) in L02 cells with caspase-1 inhibitor Ac-YVAD-cmk (AC, 50 μM) followed by LPS + GCDCA (200 μM, 24 h). ( E ) LDH release in L02 cells with AC pretreatment. (F)Western blot analysis of pyroptosis-related proteins in L02 cells with AC pretreatment. n ≥ 3 for each group. a P < 0.005, b P < 0.0001.

Journal: Journal of Inflammation Research

Article Title: Glycochenodeoxycholic acid induces the release of IL-1beta from L02 cells via the NLRP3/caspase-1/GSDMD pathway to activate LX2 cells

doi: 10.2147/JIR.S532042

Figure Lengend Snippet: GCDCA triggers caspase-1-dependent pyroptosis in hepatocytes. ( A and B ) Caspase-1/4 activity in LPS-primed L02 cells treated with GCDCA. ( C and D ) Flow cytometry quantification of pyroptotic cells (Annexin V⁺/PI⁺) in L02 cells with caspase-1 inhibitor Ac-YVAD-cmk (AC, 50 μM) followed by LPS + GCDCA (200 μM, 24 h). ( E ) LDH release in L02 cells with AC pretreatment. (F)Western blot analysis of pyroptosis-related proteins in L02 cells with AC pretreatment. n ≥ 3 for each group. a P < 0.005, b P < 0.0001.

Techniques: Activity Assay, Flow Cytometry, Western Blot

GCDCA drives IL-1β secretion through GSDMD-dependent activation. ( A ) Dose-dependent IL-1β secretion in LPS-primed L02 cells treated with GCDCA (50–400 μM, 24 h). ( B )Time-dependent IL-1β secretion (200 μM GCDCA, 12–72 h). ( C ) Western blot analysis of GSDMD-NT and GSDMD in L02 cells and mature IL-1β in cell supernatant. ( D ) ELISA quantification of extracellular IL-1β. n ≥ 3 for each group. a P < 0.01.

Journal: Journal of Inflammation Research

Article Title: Glycochenodeoxycholic acid induces the release of IL-1beta from L02 cells via the NLRP3/caspase-1/GSDMD pathway to activate LX2 cells

doi: 10.2147/JIR.S532042

Figure Lengend Snippet: GCDCA drives IL-1β secretion through GSDMD-dependent activation. ( A ) Dose-dependent IL-1β secretion in LPS-primed L02 cells treated with GCDCA (50–400 μM, 24 h). ( B )Time-dependent IL-1β secretion (200 μM GCDCA, 12–72 h). ( C ) Western blot analysis of GSDMD-NT and GSDMD in L02 cells and mature IL-1β in cell supernatant. ( D ) ELISA quantification of extracellular IL-1β. n ≥ 3 for each group. a P < 0.01.

Techniques: Activation Assay, Western Blot, Enzyme-linked Immunosorbent Assay

GCDCA-mediated hepatocyte IL-1β secretion activates HSCs. ( A ) Western blot analysis ofα-SMA and Collagen-I in LX2 cells treated with conditioned medium (CM) from GCDCA/LPS-stimulated L02 hepatocytes. ( B ) The protein levels of α-SMA and Collagen-I in LX2 cells with treatment of IL-1 receptor antagonist (IL-1RA, 200 ng/mL) upon CM exposure. ( C and D ) Representative images and quantification of LX2 migration upon CM exposure detected by wound healing assay. ( E ) CCK-8 assay of LX2 proliferation by CM treatment. n ≥ 3 for each group. a P < 0.05.

Journal: Journal of Inflammation Research

Article Title: Glycochenodeoxycholic acid induces the release of IL-1beta from L02 cells via the NLRP3/caspase-1/GSDMD pathway to activate LX2 cells

doi: 10.2147/JIR.S532042

Figure Lengend Snippet: GCDCA-mediated hepatocyte IL-1β secretion activates HSCs. ( A ) Western blot analysis ofα-SMA and Collagen-I in LX2 cells treated with conditioned medium (CM) from GCDCA/LPS-stimulated L02 hepatocytes. ( B ) The protein levels of α-SMA and Collagen-I in LX2 cells with treatment of IL-1 receptor antagonist (IL-1RA, 200 ng/mL) upon CM exposure. ( C and D ) Representative images and quantification of LX2 migration upon CM exposure detected by wound healing assay. ( E ) CCK-8 assay of LX2 proliferation by CM treatment. n ≥ 3 for each group. a P < 0.05.

Techniques: Western Blot, Migration, Wound Healing Assay, CCK-8 Assay

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