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InvivoGen nlrp3 inhibitor mcc950

GR actions over the repression of pro‐inflammatory genes requires a more accessible chromatin landscape in response to glucocorticoids in macrophages. (A) Volcano plot from RNA‐seq data in which each dot in red represents the differentially expressed genes (DEG) by Dex in LPS‐primed macrophages versus LPS‐treated with adjusted p < 0.05. The circle highlights a group of inflammasome‐associated genes. Schematic representation of the experimental setup for Dex treatment after LPS‐priming (B) and LPS plus Dex as a co‐treatment (co‐tx) (C). (D) Assessment of mRNA levels of <t>Nlrp3,</t> Nos2 , Acod1/Irg1, Il1b, Hif1a, P2ry2, Dusp1 , and Tsc22d3/Gilz genes in BMDM from Vehicle, Dex, LPS, Dex after LPS‐priming (after), and LPS plus Dex as a co‐treatment (co‐tx). The relative mRNA expression levels of the target genes were normalized to Ppib . (E) Immunoblot and densitometry analysis representing the levels of NLRP3, iNOS, ACOD1, and Pro‐IL1B in cell lysates from BMDMs, comparing the stimulation by 100 nM Dex at 6, 12, and 24 h in LPS‐primed macrophages (LPS → Dex) and as a cotreatment with LPS (LPS + Dex) as depicted in (B) and (C). (F) Meta‐profiles of GR signals over active TSSs and heatmaps depicting relative changes in Cut&Tag signal for GR enrichment in LPS, LPS plus Dex, and Dex after LPS treatments. Venn diagram illustrating the numbers of GR peaks in LPS plus Dex (LPS + Dex) and Dex after LPS (LPS → Dex) regimens. (G) Browser image of Cut&Tag signal for GR peaks over Per1 , Dusp1 , Ccl3 , Ccl4 , and Nlrp3 genes as induced and reduced by Dex treatment. (H) Frequency distribution graph for motifs enrichment analysis. The x ‐axis is the ratio of % GR peaks over % background regions, and the y ‐axis represents the −log10 of the p value. NHR: Nuclear hormone receptor. Data are mean ± SEM. Blots are representative of a minimum of 3 independent experiments. Statistical analysis was performed using one‐way ANOVA with Tukey's multiple‐comparison test (A) and (B). * p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001.

Nlrp3 Inhibitor Mcc950, supplied by InvivoGen, used in various techniques. Bioz Stars score: 96/100, based on 357 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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1) Product Images from "Timing of Glucocorticoid Treatment Dictates Glucocorticoid Receptor Actions Modulating the NLRP3‐Inflammasome Activation in Macrophages"

Article Title: Timing of Glucocorticoid Treatment Dictates Glucocorticoid Receptor Actions Modulating the NLRP3‐Inflammasome Activation in Macrophages

Journal: The FASEB Journal

doi: 10.1096/fj.202504083R

Figure Legend Snippet: GR actions over the repression of pro‐inflammatory genes requires a more accessible chromatin landscape in response to glucocorticoids in macrophages. (A) Volcano plot from RNA‐seq data in which each dot in red represents the differentially expressed genes (DEG) by Dex in LPS‐primed macrophages versus LPS‐treated with adjusted p < 0.05. The circle highlights a group of inflammasome‐associated genes. Schematic representation of the experimental setup for Dex treatment after LPS‐priming (B) and LPS plus Dex as a co‐treatment (co‐tx) (C). (D) Assessment of mRNA levels of Nlrp3, Nos2 , Acod1/Irg1, Il1b, Hif1a, P2ry2, Dusp1 , and Tsc22d3/Gilz genes in BMDM from Vehicle, Dex, LPS, Dex after LPS‐priming (after), and LPS plus Dex as a co‐treatment (co‐tx). The relative mRNA expression levels of the target genes were normalized to Ppib . (E) Immunoblot and densitometry analysis representing the levels of NLRP3, iNOS, ACOD1, and Pro‐IL1B in cell lysates from BMDMs, comparing the stimulation by 100 nM Dex at 6, 12, and 24 h in LPS‐primed macrophages (LPS → Dex) and as a cotreatment with LPS (LPS + Dex) as depicted in (B) and (C). (F) Meta‐profiles of GR signals over active TSSs and heatmaps depicting relative changes in Cut&Tag signal for GR enrichment in LPS, LPS plus Dex, and Dex after LPS treatments. Venn diagram illustrating the numbers of GR peaks in LPS plus Dex (LPS + Dex) and Dex after LPS (LPS → Dex) regimens. (G) Browser image of Cut&Tag signal for GR peaks over Per1 , Dusp1 , Ccl3 , Ccl4 , and Nlrp3 genes as induced and reduced by Dex treatment. (H) Frequency distribution graph for motifs enrichment analysis. The x ‐axis is the ratio of % GR peaks over % background regions, and the y ‐axis represents the −log10 of the p value. NHR: Nuclear hormone receptor. Data are mean ± SEM. Blots are representative of a minimum of 3 independent experiments. Statistical analysis was performed using one‐way ANOVA with Tukey's multiple‐comparison test (A) and (B). * p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001.

Techniques Used: RNA Sequencing, Expressing, Western Blot, Comparison

Glucocorticoids modulate inflammation and pyroptosis by regulating late NLRP3‐inflammasome activation through ACOD1 and iNOS. (A) Schematic representation of the experimental setup for conventional NLRP3‐inflammasome activation (upper), and late NLRP3‐inflammasome activation regulated by Dex and MCC950 (lower). (B) and (C) Quantification of IL‐1β concentration determined by ELISA in the supernatant of WT and GRKO BDMDs stimulated with LPS for 3 h (conventional) and 24 h (late), with Dex and vehicle added during the final 2 and 8 h of treatment, followed by ATP (5 mM) or Nigericin (10 μM) ( n = 3). (D) Immunoblot analysis depicting Dex effects on the protein levels of ACOD1, iNOS, NLRP3, pro‐IL‐1β, Caspase‐1 and GSDM‐D during late LPS‐induced NLRP3‐inflammasome activation and using ATP as signal 2 in WT and GRKO BMDMs lysates, detected with specific antibodies using western blotting. (E) Densitometry values of the immunoreactive bands quantified for protein content, normalized to β‐actin as depicted in (D) ( n = 4). (F) Nitrite levels in the supernatants of WT and GRKO BMDMs as depicted in (D) determined by colorimetric assay ( n = 4). (G) Assessment of lactate dehydrogenase (LDH) activity in the supernatants of WT and GRKO BMDMs as depicted in (D) ( n = 4). (H) Immunoblot analysis depicting the protein levels of NRF2 as depicted in (D) in presence of the proteasome inhibitor MG‐132 (2 μM) 6 h before harvesting cells ( n = 3). (I) Immunoblot analysis depicting the protein levels of HIF‐1α as depicted in (D) in presence of the prolyl‐hydroxylase inhibitor Roxadustat (RXD; 10 μM) 2 h before adding Dex ( n = 3). (J) Quantification of IL‐1β concentration determined by ELISA in the supernatant of WT BDMDs as depicted in (H) and (I) ( n = 3). (K) Assessment of lactate dehydrogenase (LDH) activity in supernatants of WT BMDMs subjected to the conditions described in (H) and (I) ( n = 3). Data represented as mean ± SEM. Blots shown are representative of a minimum of 3 independent experiments. Statistical analysis was performed using 2‐way ANOVA with Sidak's multiple‐comparison test (B–I); one‐way ANOVA with Tukey's multiple‐comparison test (J) and (K). * p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001.

Figure Legend Snippet: Glucocorticoids modulate inflammation and pyroptosis by regulating late NLRP3‐inflammasome activation through ACOD1 and iNOS. (A) Schematic representation of the experimental setup for conventional NLRP3‐inflammasome activation (upper), and late NLRP3‐inflammasome activation regulated by Dex and MCC950 (lower). (B) and (C) Quantification of IL‐1β concentration determined by ELISA in the supernatant of WT and GRKO BDMDs stimulated with LPS for 3 h (conventional) and 24 h (late), with Dex and vehicle added during the final 2 and 8 h of treatment, followed by ATP (5 mM) or Nigericin (10 μM) ( n = 3). (D) Immunoblot analysis depicting Dex effects on the protein levels of ACOD1, iNOS, NLRP3, pro‐IL‐1β, Caspase‐1 and GSDM‐D during late LPS‐induced NLRP3‐inflammasome activation and using ATP as signal 2 in WT and GRKO BMDMs lysates, detected with specific antibodies using western blotting. (E) Densitometry values of the immunoreactive bands quantified for protein content, normalized to β‐actin as depicted in (D) ( n = 4). (F) Nitrite levels in the supernatants of WT and GRKO BMDMs as depicted in (D) determined by colorimetric assay ( n = 4). (G) Assessment of lactate dehydrogenase (LDH) activity in the supernatants of WT and GRKO BMDMs as depicted in (D) ( n = 4). (H) Immunoblot analysis depicting the protein levels of NRF2 as depicted in (D) in presence of the proteasome inhibitor MG‐132 (2 μM) 6 h before harvesting cells ( n = 3). (I) Immunoblot analysis depicting the protein levels of HIF‐1α as depicted in (D) in presence of the prolyl‐hydroxylase inhibitor Roxadustat (RXD; 10 μM) 2 h before adding Dex ( n = 3). (J) Quantification of IL‐1β concentration determined by ELISA in the supernatant of WT BDMDs as depicted in (H) and (I) ( n = 3). (K) Assessment of lactate dehydrogenase (LDH) activity in supernatants of WT BMDMs subjected to the conditions described in (H) and (I) ( n = 3). Data represented as mean ± SEM. Blots shown are representative of a minimum of 3 independent experiments. Statistical analysis was performed using 2‐way ANOVA with Sidak's multiple‐comparison test (B–I); one‐way ANOVA with Tukey's multiple‐comparison test (J) and (K). * p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001.

Techniques Used: Activation Assay, Concentration Assay, Enzyme-linked Immunosorbent Assay, Western Blot, Colorimetric Assay, Activity Assay, Comparison

Clinically relevant course of glucocorticoid plays a role in suppressing sustained NLRP3‐Inflammasome activation. (A) Assessment of mRNA levels of Nos2 , Acod1/Irg1, Il1b, Nlrp3, Hif1a, Nrf2, P2ry2 , Drp1, Mfn2 , and Dusp1 genes during late LPS‐induced NLRP3‐inflammasome activation and using ATP as signal 2 in WT BDMDs using Dex after LPS‐priming (blue) and LPS plus Dex as a co‐treatment (red). (B) Immunoblot analysis depicting Dex effects when is added after LPS priming (LPS → Dex) or as a co‐treatment (LPS + Dex) on the protein levels of ACOD1, iNOS, NLRP3, DRP‐1, MFN2, NT‐GSDMD, pro‐IL‐1β and DUSP1/MKP1 during the late LPS‐induced NLRP3‐inflammasome activation post ATP. (C) Quantification of IL‐1β determined by ELISA in the supernatant of BMDMs as depicted in (B). (D) Assessment of lactate dehydrogenase (LDH) activity in the supernatants of BMDMs as depicted in (B) ( n = 3). (E) Nitrite levels determined by colorimetric assay in the supernatants of BMDMs as depicted in (B) ( n = 4). Data represented as mean ± SEM. Blots shown are representative of a minimum of 3 independent experiments. Statistical analysis was performed using one‐way ANOVA with Tukey's multiple‐comparison test for (A) and (C–E) and 2‐way ANOVA with Sidak's multiple‐comparison test (B). * p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001.

Figure Legend Snippet: Clinically relevant course of glucocorticoid plays a role in suppressing sustained NLRP3‐Inflammasome activation. (A) Assessment of mRNA levels of Nos2 , Acod1/Irg1, Il1b, Nlrp3, Hif1a, Nrf2, P2ry2 , Drp1, Mfn2 , and Dusp1 genes during late LPS‐induced NLRP3‐inflammasome activation and using ATP as signal 2 in WT BDMDs using Dex after LPS‐priming (blue) and LPS plus Dex as a co‐treatment (red). (B) Immunoblot analysis depicting Dex effects when is added after LPS priming (LPS → Dex) or as a co‐treatment (LPS + Dex) on the protein levels of ACOD1, iNOS, NLRP3, DRP‐1, MFN2, NT‐GSDMD, pro‐IL‐1β and DUSP1/MKP1 during the late LPS‐induced NLRP3‐inflammasome activation post ATP. (C) Quantification of IL‐1β determined by ELISA in the supernatant of BMDMs as depicted in (B). (D) Assessment of lactate dehydrogenase (LDH) activity in the supernatants of BMDMs as depicted in (B) ( n = 3). (E) Nitrite levels determined by colorimetric assay in the supernatants of BMDMs as depicted in (B) ( n = 4). Data represented as mean ± SEM. Blots shown are representative of a minimum of 3 independent experiments. Statistical analysis was performed using one‐way ANOVA with Tukey's multiple‐comparison test for (A) and (C–E) and 2‐way ANOVA with Sidak's multiple‐comparison test (B). * p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001.

Techniques Used: Activation Assay, Western Blot, Enzyme-linked Immunosorbent Assay, Activity Assay, Colorimetric Assay, Comparison

The loss of Glucocorticoid Receptor (GR) in murine myeloid cells and the block of GR signaling in human monocytes‐derived macrophages exacerbates the NLRP3 inflammasome activation. (A) Schematic representation of the experimental setup for in vivo peritonitis model using MSU crystal. Peritoneal lavage fluid was collected 6 h post‐ intraperitoneal injection of 30 mg/kg MSU crystals in WT and myeloid‐GRKO mice. Peritoneal lavage involved the injection of 2.5 mL PBS and subsequent retrieval from the peritoneal cavity for supernatant harvesting and immune cells isolation. (B) Evaluation of IL‐1β concentration in peritoneal lavage. (C) Determination of absolute numbers of infiltrating neutrophils in peritoneal lavage, as was described in (A), calculated based on cell count per mL and the total recovered volume. (D) Relative percentage of small peritoneal macrophages (SPM) and (E) large peritoneal macrophages (LPM) expressing differentially the markers F4/80 and MHC‐II. These cell populations were gated from CD11b + /CD115 + cells. Data represented as mean ± SEM ( n = 9, from B to E, where each dot representing one mouse, encompassing both female and male). (F) Schematic representation of the experimental setup for late NLRP3‐inflammasome activation in human monocytes‐derived macrophages (MDMs) modulated by Dex in the presence of the GR antagonist RU‐486. (G) Quantification of NLRP3 normalized to β‐actin in lysates from human MDMs stimulated with LPS for 24 h, with the addition of the antagonist RU‐486 and Dex during the final 8 h, followed by ATP (5 mM). (H) Quantification of ACOD1 protein as depicted in (G). (I) Quantification of pro‐IL‐1β protein as depicted in (G). (J) Assessment of IL‐1β secretion in human MDMs stimulated as described in (G), determined by ELISA ( N = 6). Data representative of 4–6 healthy donors. Statistical analysis was performed using two‐tailed unpaired t ‐tests (B–E) and one‐way ANOVA with Tukey's multiple‐comparison test (G–J) * p < 0.05; ** p < 0.01.

Figure Legend Snippet: The loss of Glucocorticoid Receptor (GR) in murine myeloid cells and the block of GR signaling in human monocytes‐derived macrophages exacerbates the NLRP3 inflammasome activation. (A) Schematic representation of the experimental setup for in vivo peritonitis model using MSU crystal. Peritoneal lavage fluid was collected 6 h post‐ intraperitoneal injection of 30 mg/kg MSU crystals in WT and myeloid‐GRKO mice. Peritoneal lavage involved the injection of 2.5 mL PBS and subsequent retrieval from the peritoneal cavity for supernatant harvesting and immune cells isolation. (B) Evaluation of IL‐1β concentration in peritoneal lavage. (C) Determination of absolute numbers of infiltrating neutrophils in peritoneal lavage, as was described in (A), calculated based on cell count per mL and the total recovered volume. (D) Relative percentage of small peritoneal macrophages (SPM) and (E) large peritoneal macrophages (LPM) expressing differentially the markers F4/80 and MHC‐II. These cell populations were gated from CD11b + /CD115 + cells. Data represented as mean ± SEM ( n = 9, from B to E, where each dot representing one mouse, encompassing both female and male). (F) Schematic representation of the experimental setup for late NLRP3‐inflammasome activation in human monocytes‐derived macrophages (MDMs) modulated by Dex in the presence of the GR antagonist RU‐486. (G) Quantification of NLRP3 normalized to β‐actin in lysates from human MDMs stimulated with LPS for 24 h, with the addition of the antagonist RU‐486 and Dex during the final 8 h, followed by ATP (5 mM). (H) Quantification of ACOD1 protein as depicted in (G). (I) Quantification of pro‐IL‐1β protein as depicted in (G). (J) Assessment of IL‐1β secretion in human MDMs stimulated as described in (G), determined by ELISA ( N = 6). Data representative of 4–6 healthy donors. Statistical analysis was performed using two‐tailed unpaired t ‐tests (B–E) and one‐way ANOVA with Tukey's multiple‐comparison test (G–J) * p < 0.05; ** p < 0.01.

Techniques Used: Blocking Assay, Derivative Assay, Activation Assay, In Vivo, Injection, Isolation, Concentration Assay, Cell Characterization, Expressing, Enzyme-linked Immunosorbent Assay, Two Tailed Test, Comparison

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Journal: The FASEB Journal

Article Title: Timing of Glucocorticoid Treatment Dictates Glucocorticoid Receptor Actions Modulating the NLRP3‐Inflammasome Activation in Macrophages

doi: 10.1096/fj.202504083R

Figure Lengend Snippet: GR actions over the repression of pro‐inflammatory genes requires a more accessible chromatin landscape in response to glucocorticoids in macrophages. (A) Volcano plot from RNA‐seq data in which each dot in red represents the differentially expressed genes (DEG) by Dex in LPS‐primed macrophages versus LPS‐treated with adjusted p < 0.05. The circle highlights a group of inflammasome‐associated genes. Schematic representation of the experimental setup for Dex treatment after LPS‐priming (B) and LPS plus Dex as a co‐treatment (co‐tx) (C). (D) Assessment of mRNA levels of Nlrp3, Nos2 , Acod1/Irg1, Il1b, Hif1a, P2ry2, Dusp1 , and Tsc22d3/Gilz genes in BMDM from Vehicle, Dex, LPS, Dex after LPS‐priming (after), and LPS plus Dex as a co‐treatment (co‐tx). The relative mRNA expression levels of the target genes were normalized to Ppib . (E) Immunoblot and densitometry analysis representing the levels of NLRP3, iNOS, ACOD1, and Pro‐IL1B in cell lysates from BMDMs, comparing the stimulation by 100 nM Dex at 6, 12, and 24 h in LPS‐primed macrophages (LPS → Dex) and as a cotreatment with LPS (LPS + Dex) as depicted in (B) and (C). (F) Meta‐profiles of GR signals over active TSSs and heatmaps depicting relative changes in Cut&Tag signal for GR enrichment in LPS, LPS plus Dex, and Dex after LPS treatments. Venn diagram illustrating the numbers of GR peaks in LPS plus Dex (LPS + Dex) and Dex after LPS (LPS → Dex) regimens. (G) Browser image of Cut&Tag signal for GR peaks over Per1 , Dusp1 , Ccl3 , Ccl4 , and Nlrp3 genes as induced and reduced by Dex treatment. (H) Frequency distribution graph for motifs enrichment analysis. The x ‐axis is the ratio of % GR peaks over % background regions, and the y ‐axis represents the −log10 of the p value. NHR: Nuclear hormone receptor. Data are mean ± SEM. Blots are representative of a minimum of 3 independent experiments. Statistical analysis was performed using one‐way ANOVA with Tukey's multiple‐comparison test (A) and (B). * p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001.

Article Snippet: Lipopolysaccharide from E. coli 0111: B4 strain (LPS‐EB), NLRP3 inhibitor MCC950, Caspase‐1 inhibitor Ac‐Y‐VAD‐cmk, 4‐octyl‐itaconate (4‐OI), adenosine 5′‐triphosphate disodium salt (ATP), nigericin, and monosodium urate (MSU) crystals were purchased from InvivoGen (San Diego, CA, USA).

Techniques: RNA Sequencing, Expressing, Western Blot, Comparison

Journal: The FASEB Journal

Article Title: Timing of Glucocorticoid Treatment Dictates Glucocorticoid Receptor Actions Modulating the NLRP3‐Inflammasome Activation in Macrophages

doi: 10.1096/fj.202504083R

Figure Lengend Snippet: Glucocorticoids modulate inflammation and pyroptosis by regulating late NLRP3‐inflammasome activation through ACOD1 and iNOS. (A) Schematic representation of the experimental setup for conventional NLRP3‐inflammasome activation (upper), and late NLRP3‐inflammasome activation regulated by Dex and MCC950 (lower). (B) and (C) Quantification of IL‐1β concentration determined by ELISA in the supernatant of WT and GRKO BDMDs stimulated with LPS for 3 h (conventional) and 24 h (late), with Dex and vehicle added during the final 2 and 8 h of treatment, followed by ATP (5 mM) or Nigericin (10 μM) ( n = 3). (D) Immunoblot analysis depicting Dex effects on the protein levels of ACOD1, iNOS, NLRP3, pro‐IL‐1β, Caspase‐1 and GSDM‐D during late LPS‐induced NLRP3‐inflammasome activation and using ATP as signal 2 in WT and GRKO BMDMs lysates, detected with specific antibodies using western blotting. (E) Densitometry values of the immunoreactive bands quantified for protein content, normalized to β‐actin as depicted in (D) ( n = 4). (F) Nitrite levels in the supernatants of WT and GRKO BMDMs as depicted in (D) determined by colorimetric assay ( n = 4). (G) Assessment of lactate dehydrogenase (LDH) activity in the supernatants of WT and GRKO BMDMs as depicted in (D) ( n = 4). (H) Immunoblot analysis depicting the protein levels of NRF2 as depicted in (D) in presence of the proteasome inhibitor MG‐132 (2 μM) 6 h before harvesting cells ( n = 3). (I) Immunoblot analysis depicting the protein levels of HIF‐1α as depicted in (D) in presence of the prolyl‐hydroxylase inhibitor Roxadustat (RXD; 10 μM) 2 h before adding Dex ( n = 3). (J) Quantification of IL‐1β concentration determined by ELISA in the supernatant of WT BDMDs as depicted in (H) and (I) ( n = 3). (K) Assessment of lactate dehydrogenase (LDH) activity in supernatants of WT BMDMs subjected to the conditions described in (H) and (I) ( n = 3). Data represented as mean ± SEM. Blots shown are representative of a minimum of 3 independent experiments. Statistical analysis was performed using 2‐way ANOVA with Sidak's multiple‐comparison test (B–I); one‐way ANOVA with Tukey's multiple‐comparison test (J) and (K). * p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001.

Techniques: Activation Assay, Concentration Assay, Enzyme-linked Immunosorbent Assay, Western Blot, Colorimetric Assay, Activity Assay, Comparison

Journal: The FASEB Journal

Article Title: Timing of Glucocorticoid Treatment Dictates Glucocorticoid Receptor Actions Modulating the NLRP3‐Inflammasome Activation in Macrophages

doi: 10.1096/fj.202504083R

Figure Lengend Snippet: Clinically relevant course of glucocorticoid plays a role in suppressing sustained NLRP3‐Inflammasome activation. (A) Assessment of mRNA levels of Nos2 , Acod1/Irg1, Il1b, Nlrp3, Hif1a, Nrf2, P2ry2 , Drp1, Mfn2 , and Dusp1 genes during late LPS‐induced NLRP3‐inflammasome activation and using ATP as signal 2 in WT BDMDs using Dex after LPS‐priming (blue) and LPS plus Dex as a co‐treatment (red). (B) Immunoblot analysis depicting Dex effects when is added after LPS priming (LPS → Dex) or as a co‐treatment (LPS + Dex) on the protein levels of ACOD1, iNOS, NLRP3, DRP‐1, MFN2, NT‐GSDMD, pro‐IL‐1β and DUSP1/MKP1 during the late LPS‐induced NLRP3‐inflammasome activation post ATP. (C) Quantification of IL‐1β determined by ELISA in the supernatant of BMDMs as depicted in (B). (D) Assessment of lactate dehydrogenase (LDH) activity in the supernatants of BMDMs as depicted in (B) ( n = 3). (E) Nitrite levels determined by colorimetric assay in the supernatants of BMDMs as depicted in (B) ( n = 4). Data represented as mean ± SEM. Blots shown are representative of a minimum of 3 independent experiments. Statistical analysis was performed using one‐way ANOVA with Tukey's multiple‐comparison test for (A) and (C–E) and 2‐way ANOVA with Sidak's multiple‐comparison test (B). * p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001.

Techniques: Activation Assay, Western Blot, Enzyme-linked Immunosorbent Assay, Activity Assay, Colorimetric Assay, Comparison

Journal: The FASEB Journal

Article Title: Timing of Glucocorticoid Treatment Dictates Glucocorticoid Receptor Actions Modulating the NLRP3‐Inflammasome Activation in Macrophages

doi: 10.1096/fj.202504083R

Figure Lengend Snippet: The loss of Glucocorticoid Receptor (GR) in murine myeloid cells and the block of GR signaling in human monocytes‐derived macrophages exacerbates the NLRP3 inflammasome activation. (A) Schematic representation of the experimental setup for in vivo peritonitis model using MSU crystal. Peritoneal lavage fluid was collected 6 h post‐ intraperitoneal injection of 30 mg/kg MSU crystals in WT and myeloid‐GRKO mice. Peritoneal lavage involved the injection of 2.5 mL PBS and subsequent retrieval from the peritoneal cavity for supernatant harvesting and immune cells isolation. (B) Evaluation of IL‐1β concentration in peritoneal lavage. (C) Determination of absolute numbers of infiltrating neutrophils in peritoneal lavage, as was described in (A), calculated based on cell count per mL and the total recovered volume. (D) Relative percentage of small peritoneal macrophages (SPM) and (E) large peritoneal macrophages (LPM) expressing differentially the markers F4/80 and MHC‐II. These cell populations were gated from CD11b + /CD115 + cells. Data represented as mean ± SEM ( n = 9, from B to E, where each dot representing one mouse, encompassing both female and male). (F) Schematic representation of the experimental setup for late NLRP3‐inflammasome activation in human monocytes‐derived macrophages (MDMs) modulated by Dex in the presence of the GR antagonist RU‐486. (G) Quantification of NLRP3 normalized to β‐actin in lysates from human MDMs stimulated with LPS for 24 h, with the addition of the antagonist RU‐486 and Dex during the final 8 h, followed by ATP (5 mM). (H) Quantification of ACOD1 protein as depicted in (G). (I) Quantification of pro‐IL‐1β protein as depicted in (G). (J) Assessment of IL‐1β secretion in human MDMs stimulated as described in (G), determined by ELISA ( N = 6). Data representative of 4–6 healthy donors. Statistical analysis was performed using two‐tailed unpaired t ‐tests (B–E) and one‐way ANOVA with Tukey's multiple‐comparison test (G–J) * p < 0.05; ** p < 0.01.

Techniques: Blocking Assay, Derivative Assay, Activation Assay, In Vivo, Injection, Isolation, Concentration Assay, Cell Characterization, Expressing, Enzyme-linked Immunosorbent Assay, Two Tailed Test, Comparison

LYC attenuated DON-induced pyroptosis and up-regulation of TXNIP protein in the IPEC-J2 cells. (A) Expression of pyroptosis-related proteins. (B) The relative level of NLRP3, IL-1β, Caspase-1, GSDMD-N, and TXNIP proteins. (C) Representative IF images of NLRP3. (D) PCA. (E) Chord diagrams. (F) Molecular docking simulation for the ligand−protein binding of DON with TXNIP. (G) RMSD of the complex. (H) Rg number. (I) Gibbs free energy 2D landscape. (J) RMSF number. (K) CETSA. (L) The relative level of TXNIP intensity. Data are presented as the mean ± SD. Symbol for the significance of differences between the CON group and DON group: *** P < 0.001. Symbol for the significance of differences between the DON group and LDO group: ### P < 0.001.

Journal: Research

Article Title: Lycopene Antagonizes Deoxynivalenol-Induced Porcine Intestinal Epithelial Cell Senescence by Inhibiting TXNIP-Mediated NLRP3 Inflammasome Activation

doi: 10.34133/research.1090

Figure Lengend Snippet: LYC attenuated DON-induced pyroptosis and up-regulation of TXNIP protein in the IPEC-J2 cells. (A) Expression of pyroptosis-related proteins. (B) The relative level of NLRP3, IL-1β, Caspase-1, GSDMD-N, and TXNIP proteins. (C) Representative IF images of NLRP3. (D) PCA. (E) Chord diagrams. (F) Molecular docking simulation for the ligand−protein binding of DON with TXNIP. (G) RMSD of the complex. (H) Rg number. (I) Gibbs free energy 2D landscape. (J) RMSF number. (K) CETSA. (L) The relative level of TXNIP intensity. Data are presented as the mean ± SD. Symbol for the significance of differences between the CON group and DON group: *** P < 0.001. Symbol for the significance of differences between the DON group and LDO group: ### P < 0.001.

Article Snippet: The NLRP3 inhibitor MCC950 (MedChemExpress, USA) was employed to inhibit the NLRP3 inflammasome at a concentration of 10 nM.

Techniques: Expressing, Protein Binding

TXNIP overexpression counteracted the protective effects of LYC on DON-induced inflammatory responses and pyroptosis. (A) Expression of inflammation-related proteins. (B) The relative level of TLR4, MyD88, TNF-α, IL-6, p-NF-κB, and p-IκB proteins. (C) PCA. (D) Expression of pyroptosis-related proteins. (E) The relative level of NLRP3, IL-1β, Caspase-1, GSDMD-N, and TXNIP proteins. (F) Representative IF images of p-IκB. (G) Representative IF images of NLRP3. Data are presented as the mean ± SD. Symbol for the significance of differences between the CON group and DON group: * P < 0.05, ** P < 0.01, *** P < 0.001. Symbol for the significance of differences between the LDO group and LDO + TXNIP group: ## P < 0.01, ### P < 0.001.

Journal: Research

Article Title: Lycopene Antagonizes Deoxynivalenol-Induced Porcine Intestinal Epithelial Cell Senescence by Inhibiting TXNIP-Mediated NLRP3 Inflammasome Activation

doi: 10.34133/research.1090

Figure Lengend Snippet: TXNIP overexpression counteracted the protective effects of LYC on DON-induced inflammatory responses and pyroptosis. (A) Expression of inflammation-related proteins. (B) The relative level of TLR4, MyD88, TNF-α, IL-6, p-NF-κB, and p-IκB proteins. (C) PCA. (D) Expression of pyroptosis-related proteins. (E) The relative level of NLRP3, IL-1β, Caspase-1, GSDMD-N, and TXNIP proteins. (F) Representative IF images of p-IκB. (G) Representative IF images of NLRP3. Data are presented as the mean ± SD. Symbol for the significance of differences between the CON group and DON group: * P < 0.05, ** P < 0.01, *** P < 0.001. Symbol for the significance of differences between the LDO group and LDO + TXNIP group: ## P < 0.01, ### P < 0.001.

Article Snippet: The NLRP3 inhibitor MCC950 (MedChemExpress, USA) was employed to inhibit the NLRP3 inflammasome at a concentration of 10 nM.

Techniques: Over Expression, Expressing

LYC relieved DON-induced senescence by inhibiting TXNIP-mediated NLRP3 inflammasome activation. (A) Expression of senescence-related proteins. (B) The relative level of Ki-67, P21, P16, P53, and γH2AX proteins. (C) SA-β-galactosidase. (D) EdU staining. (E) Flow cytometric analysis of cell cycle distribution. (F) Representative IF images of γH2AX, P53, Ki-67, and P16. (G) Correlation analysis. (H) PPI network. Data are presented as the mean ± SD. Symbol for the significance of differences between the LDO + TXNIP group and the LDO + TXNIP + MCC950: * P < 0.005, ** P < 0.01, *** P < 0.001.

Journal: Research

Article Title: Lycopene Antagonizes Deoxynivalenol-Induced Porcine Intestinal Epithelial Cell Senescence by Inhibiting TXNIP-Mediated NLRP3 Inflammasome Activation

doi: 10.34133/research.1090

Figure Lengend Snippet: LYC relieved DON-induced senescence by inhibiting TXNIP-mediated NLRP3 inflammasome activation. (A) Expression of senescence-related proteins. (B) The relative level of Ki-67, P21, P16, P53, and γH2AX proteins. (C) SA-β-galactosidase. (D) EdU staining. (E) Flow cytometric analysis of cell cycle distribution. (F) Representative IF images of γH2AX, P53, Ki-67, and P16. (G) Correlation analysis. (H) PPI network. Data are presented as the mean ± SD. Symbol for the significance of differences between the LDO + TXNIP group and the LDO + TXNIP + MCC950: * P < 0.005, ** P < 0.01, *** P < 0.001.

Article Snippet: The NLRP3 inhibitor MCC950 (MedChemExpress, USA) was employed to inhibit the NLRP3 inflammasome at a concentration of 10 nM.

Techniques: Activation Assay, Expressing, Staining

LYC antagonized DON-induced disruption of the interaction between TXNIP and NLRP3 by binding to TXNIP, inhibited NLRP3 activation and pyroptosis, and thus effectively delayed intestinal epithelium senescence. TXNIP can serve as a target for regulating mycotoxin-induced intestinal epithelium senescence and a fresh perspective into antagonizing pyroptosis.

Journal: Research

Article Title: Lycopene Antagonizes Deoxynivalenol-Induced Porcine Intestinal Epithelial Cell Senescence by Inhibiting TXNIP-Mediated NLRP3 Inflammasome Activation

doi: 10.34133/research.1090

Figure Lengend Snippet: LYC antagonized DON-induced disruption of the interaction between TXNIP and NLRP3 by binding to TXNIP, inhibited NLRP3 activation and pyroptosis, and thus effectively delayed intestinal epithelium senescence. TXNIP can serve as a target for regulating mycotoxin-induced intestinal epithelium senescence and a fresh perspective into antagonizing pyroptosis.

Article Snippet: The NLRP3 inhibitor MCC950 (MedChemExpress, USA) was employed to inhibit the NLRP3 inflammasome at a concentration of 10 nM.

Techniques: Disruption, Binding Assay, Activation Assay

Review

Structured Review

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1) Product Images from "Timing of Glucocorticoid Treatment Dictates Glucocorticoid Receptor Actions Modulating the NLRP3‐Inflammasome Activation in Macrophages"

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