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anti human il 1β (InvivoGen)

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InvivoGen anti human il 1β

<t>a,</t> <t>IL-1β</t> activity in the supernatant of THP1-WT vs. - GSDMD -KO cells treated with LPS±HPPs for 16 hours, measured using HEK-Blue™ IL-1β reporter cells (three combined experiments, error bars represent standard error, one-way ANOVA with Bonferroni test); b, LDH release from THP1-WT vs. – GSDMD -KO cells treated with LPS±HPP for 16 hours (three combined experiments, one-way ANOVA with Bonferroni test); c-d, IL-1β activity in the supernatant of THP1-WT vs. - GSDMD -KO cells © and human PBMCs (d) treated with LPS and NG±HPPs for 16 hours. measured using HEK-Blue™ IL-1β reporter cells (three combined experiments, error bars represent standard error, one-way ANOVA with Bonferroni test); e-f, LDH release from THP1-WT vs. – GSDMD -KO cells € and human PBMCs (f) treated with LPS and NG±HPPs for 16 hours (three combined experiments, one-way ANOVA with Bonferroni test).

Anti Human Il 1β, supplied by InvivoGen, used in various techniques. Bioz Stars score: 94/100, based on 21 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/anti+human+il+1%CE%B2/bio_rxiv__64898__2026__04__23__720410-259-18-25?v=InvivoGen
Average 94 stars, based on 21 article reviews

anti human il 1β - by Bioz Stars, 2026-07

94/100 stars

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1) Product Images from "Microbiome-derived hydroxyphenyl propanoates enhance antitumour immunity by potentiating gasdermin D activity in tumour-associated myeloid cells"

Article Title: Microbiome-derived hydroxyphenyl propanoates enhance antitumour immunity by potentiating gasdermin D activity in tumour-associated myeloid cells

Journal: bioRxiv

doi: 10.64898/2026.04.23.720410

a, IL-1β activity in the supernatant of THP1-WT vs. - GSDMD -KO cells treated with LPS±HPPs for 16 hours, measured using HEK-Blue™ IL-1β reporter cells (three combined experiments, error bars represent standard error, one-way ANOVA with Bonferroni test); b, LDH release from THP1-WT vs. – GSDMD -KO cells treated with LPS±HPP for 16 hours (three combined experiments, one-way ANOVA with Bonferroni test); c-d, IL-1β activity in the supernatant of THP1-WT vs. - GSDMD -KO cells © and human PBMCs (d) treated with LPS and NG±HPPs for 16 hours. measured using HEK-Blue™ IL-1β reporter cells (three combined experiments, error bars represent standard error, one-way ANOVA with Bonferroni test); e-f, LDH release from THP1-WT vs. – GSDMD -KO cells € and human PBMCs (f) treated with LPS and NG±HPPs for 16 hours (three combined experiments, one-way ANOVA with Bonferroni test).

Figure Legend Snippet: a, IL-1β activity in the supernatant of THP1-WT vs. - GSDMD -KO cells treated with LPS±HPPs for 16 hours, measured using HEK-Blue™ IL-1β reporter cells (three combined experiments, error bars represent standard error, one-way ANOVA with Bonferroni test); b, LDH release from THP1-WT vs. – GSDMD -KO cells treated with LPS±HPP for 16 hours (three combined experiments, one-way ANOVA with Bonferroni test); c-d, IL-1β activity in the supernatant of THP1-WT vs. - GSDMD -KO cells © and human PBMCs (d) treated with LPS and NG±HPPs for 16 hours. measured using HEK-Blue™ IL-1β reporter cells (three combined experiments, error bars represent standard error, one-way ANOVA with Bonferroni test); e-f, LDH release from THP1-WT vs. – GSDMD -KO cells € and human PBMCs (f) treated with LPS and NG±HPPs for 16 hours (three combined experiments, one-way ANOVA with Bonferroni test).

Techniques Used: Activity Assay

a-b, tumour growth kinetics and OS for orthotopic M3-9-M OVA tumours in male WT or Gsdmd -KO mice receiving vehicle or 3,2-HPP treatments from day 1 post cell-implantation (n =8/group; two combined experiments, two-way ANOVA test for growth kinetics, Log-Rank test for OS); c, [IL-1β] in interstitial fluid harvested from 18-day old M3-9-M OVA tumours grown in male WT or Gsdmd -KO mice receiving vehicle or 3,2-HPP treatment from day 1 post-cell implantation (two combined experiments, one-way ANOVA with Bonferroni multiple comparison test); d, GSDMD peptides quantified from a publicly available tumour proteomic database established from stage IV melanoma patients undergoing anti-PD-1 treatment (responder, R = 40 and non-responder, NR = 27); e-g, correlation uncleaved GSDMD peptide with NFKB1 gene targets and two sets of M1- vs. M2-like macrophage gene signatures, respectively, in stage IV melanoma patients undergoing anti-PD-1 treatment (R = 18 and NR = 6, chi-square test).

Figure Legend Snippet: a-b, tumour growth kinetics and OS for orthotopic M3-9-M OVA tumours in male WT or Gsdmd -KO mice receiving vehicle or 3,2-HPP treatments from day 1 post cell-implantation (n =8/group; two combined experiments, two-way ANOVA test for growth kinetics, Log-Rank test for OS); c, [IL-1β] in interstitial fluid harvested from 18-day old M3-9-M OVA tumours grown in male WT or Gsdmd -KO mice receiving vehicle or 3,2-HPP treatment from day 1 post-cell implantation (two combined experiments, one-way ANOVA with Bonferroni multiple comparison test); d, GSDMD peptides quantified from a publicly available tumour proteomic database established from stage IV melanoma patients undergoing anti-PD-1 treatment (responder, R = 40 and non-responder, NR = 27); e-g, correlation uncleaved GSDMD peptide with NFKB1 gene targets and two sets of M1- vs. M2-like macrophage gene signatures, respectively, in stage IV melanoma patients undergoing anti-PD-1 treatment (R = 18 and NR = 6, chi-square test).

Techniques Used: Comparison

Image Search Results

Journal: bioRxiv

Article Title: Microbiome-derived hydroxyphenyl propanoates enhance antitumour immunity by potentiating gasdermin D activity in tumour-associated myeloid cells

doi: 10.64898/2026.04.23.720410

Figure Lengend Snippet: a, IL-1β activity in the supernatant of THP1-WT vs. - GSDMD -KO cells treated with LPS±HPPs for 16 hours, measured using HEK-Blue™ IL-1β reporter cells (three combined experiments, error bars represent standard error, one-way ANOVA with Bonferroni test); b, LDH release from THP1-WT vs. – GSDMD -KO cells treated with LPS±HPP for 16 hours (three combined experiments, one-way ANOVA with Bonferroni test); c-d, IL-1β activity in the supernatant of THP1-WT vs. - GSDMD -KO cells © and human PBMCs (d) treated with LPS and NG±HPPs for 16 hours. measured using HEK-Blue™ IL-1β reporter cells (three combined experiments, error bars represent standard error, one-way ANOVA with Bonferroni test); e-f, LDH release from THP1-WT vs. – GSDMD -KO cells € and human PBMCs (f) treated with LPS and NG±HPPs for 16 hours (three combined experiments, one-way ANOVA with Bonferroni test).

Article Snippet: To neutralize IL-1 receptor signalling, the following antibodies were used: anti-human IL-1α (1 μg/mL; clone 7D4; mabg-hil1a-3; InvivoGen), anti-human IL-1β (1 μg/mL; clone 4H5; mabg-hil1b-3; InvivoGen) and IgG1 isotype control (1 μg/mL; clone T8E5; mabg1-ctrlm; InvivoGen).

Techniques: Activity Assay

Journal: bioRxiv

Article Title: Microbiome-derived hydroxyphenyl propanoates enhance antitumour immunity by potentiating gasdermin D activity in tumour-associated myeloid cells

doi: 10.64898/2026.04.23.720410

Figure Lengend Snippet: a-b, tumour growth kinetics and OS for orthotopic M3-9-M OVA tumours in male WT or Gsdmd -KO mice receiving vehicle or 3,2-HPP treatments from day 1 post cell-implantation (n =8/group; two combined experiments, two-way ANOVA test for growth kinetics, Log-Rank test for OS); c, [IL-1β] in interstitial fluid harvested from 18-day old M3-9-M OVA tumours grown in male WT or Gsdmd -KO mice receiving vehicle or 3,2-HPP treatment from day 1 post-cell implantation (two combined experiments, one-way ANOVA with Bonferroni multiple comparison test); d, GSDMD peptides quantified from a publicly available tumour proteomic database established from stage IV melanoma patients undergoing anti-PD-1 treatment (responder, R = 40 and non-responder, NR = 27); e-g, correlation uncleaved GSDMD peptide with NFKB1 gene targets and two sets of M1- vs. M2-like macrophage gene signatures, respectively, in stage IV melanoma patients undergoing anti-PD-1 treatment (R = 18 and NR = 6, chi-square test).

Techniques: Comparison

TMH inhibits activation of the NLRP3 inflammasome. (A) Schematic workflow of in vitro NLRP3 inflammasome activation. (B,C) Cell viability was assessed in J774A.1 cells (B) and PMA (500 nM)-differentiated THP-1 cells (C) treated with TMH for 2 or 18 h using the EZ-Cytox assay. (D) LPS-primed J774A.1 cells were treated with TMH for 2 h, then stimulated with ATP (5 mM) for 30 min in the presence or absence of MCC950. IL-1β (p17) levels in supernatants were measured by ELISA. (E,F) PMA-differentiated THP-1 cells were primed with LPS, treated with TMH for 2 h, then stimulated with ATP (5 mM) (E) or nigericin (10 μM) (F) for 1 h, with or without MCC950. IL-1β (p17) levels in supernatants were determined by ELISA. Data are presented as the mean ± SD (n = 3). Statistical analysis was performed using one-way ANOVA followed by Tukey’s multiple comparisons test. *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001; n.s., not significant.

Journal: Frontiers in Pharmacology

Article Title: Thymelaea hirsuta (L.) Endl . extract attenuates NLRP3 inflammasome activation via modulation of ATPase activity

doi: 10.3389/fphar.2026.1781860

Figure Lengend Snippet: TMH inhibits activation of the NLRP3 inflammasome. (A) Schematic workflow of in vitro NLRP3 inflammasome activation. (B,C) Cell viability was assessed in J774A.1 cells (B) and PMA (500 nM)-differentiated THP-1 cells (C) treated with TMH for 2 or 18 h using the EZ-Cytox assay. (D) LPS-primed J774A.1 cells were treated with TMH for 2 h, then stimulated with ATP (5 mM) for 30 min in the presence or absence of MCC950. IL-1β (p17) levels in supernatants were measured by ELISA. (E,F) PMA-differentiated THP-1 cells were primed with LPS, treated with TMH for 2 h, then stimulated with ATP (5 mM) (E) or nigericin (10 μM) (F) for 1 h, with or without MCC950. IL-1β (p17) levels in supernatants were determined by ELISA. Data are presented as the mean ± SD (n = 3). Statistical analysis was performed using one-way ANOVA followed by Tukey’s multiple comparisons test. *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001; n.s., not significant.

Article Snippet: Antibodies specific for human IL-1β (AF-401-NA) and mouse IL-1β (AF-201-NA) were purchased from R&D Systems (United States).

Techniques: Activation Assay, In Vitro, Enzyme-linked Immunosorbent Assay

$TMH does not affect other inflammasome or inflammatory pathways. (A,B) LPS-primed J774A.1 cells were treated with TMH for 2 h, followed by stimulation with either dsDNA (1 μg/mL) (A) or flagellin (B) transfected using Lipofectamine 2000 for 3 h. (C) Following TMH treatment (2 h), nuclear and cytosolic fractions of LPS-primed J774A.1 cells were separated and assessed for NF-κB p65 translocation by immunoblotting. (D) HEK293FT cells transfected with the pGL4.32 luciferase reporter vector were treated with TNF-α (20 ng/mL) for 5 h, with or without TMH pre-treatment (2 h). Luciferase activity was measured using the Bright-Glo™ luciferase assay system (Promega). Data are presented as the mean ± SD (n = 3). Statistical analysis was performed using one-way ANOVA followed by Tukey’s multiple comparisons test n.s., not significant.$

Journal: Frontiers in Pharmacology

Article Title: Thymelaea hirsuta (L.) Endl . extract attenuates NLRP3 inflammasome activation via modulation of ATPase activity

doi: 10.3389/fphar.2026.1781860

Figure Lengend Snippet: TMH does not affect other inflammasome or inflammatory pathways. (A,B) LPS-primed J774A.1 cells were treated with TMH for 2 h, followed by stimulation with either dsDNA (1 μg/mL) (A) or flagellin (B) transfected using Lipofectamine 2000 for 3 h. (C) Following TMH treatment (2 h), nuclear and cytosolic fractions of LPS-primed J774A.1 cells were separated and assessed for NF-κB p65 translocation by immunoblotting. (D) HEK293FT cells transfected with the pGL4.32 luciferase reporter vector were treated with TNF-α (20 ng/mL) for 5 h, with or without TMH pre-treatment (2 h). Luciferase activity was measured using the Bright-Glo™ luciferase assay system (Promega). Data are presented as the mean ± SD (n = 3). Statistical analysis was performed using one-way ANOVA followed by Tukey’s multiple comparisons test n.s., not significant.

Article Snippet: Antibodies specific for human IL-1β (AF-401-NA) and mouse IL-1β (AF-201-NA) were purchased from R&D Systems (United States).

Techniques: Transfection, Translocation Assay, Western Blot, Luciferase, Plasmid Preparation, Activity Assay

TMH inhibits NLRP3 inflammasome activation by suppressing ASC oligomerization and ATPase activity. (A) LPS-primed J774A.1 cells were treated with TMH for 2 h, then stimulated with imiquimod (200 μM) for 1 h. (B) Cells were treated with TMH (2 h), stained with MitoSOX (5 μM, 10 min), and stimulated with ATP (5 mM, 5 min). Intracellular ROS were visualized by confocal microscopy. (C,D) PMA-differentiated THP-1 cells were primed with LPS, treated with TMH for 2 h, then stimulated with nigericin (10 μM, 1 h). ASC speck formation was examined by confocal microscopy (C) , and representative images from five fields are shown (D) . (E) Cells were stimulated with or without MCC950 and cross-linked with DSS (2.5 mM, 30 min) before immunoblotting for ASC oligomerization. (F) NLRP3 ATPase activity was measured using the ADP-Glo™ assay to quantify ATP-to-ADP conversion following TMH treatment. Data are presented as the mean ± SD (n = 3). Statistical analysis was performed using one-way ANOVA followed by Tukey’s multiple comparisons test. **P < 0.01, ***P < 0.001.

Journal: Frontiers in Pharmacology

Article Title: Thymelaea hirsuta (L.) Endl . extract attenuates NLRP3 inflammasome activation via modulation of ATPase activity

doi: 10.3389/fphar.2026.1781860

Figure Lengend Snippet: TMH inhibits NLRP3 inflammasome activation by suppressing ASC oligomerization and ATPase activity. (A) LPS-primed J774A.1 cells were treated with TMH for 2 h, then stimulated with imiquimod (200 μM) for 1 h. (B) Cells were treated with TMH (2 h), stained with MitoSOX (5 μM, 10 min), and stimulated with ATP (5 mM, 5 min). Intracellular ROS were visualized by confocal microscopy. (C,D) PMA-differentiated THP-1 cells were primed with LPS, treated with TMH for 2 h, then stimulated with nigericin (10 μM, 1 h). ASC speck formation was examined by confocal microscopy (C) , and representative images from five fields are shown (D) . (E) Cells were stimulated with or without MCC950 and cross-linked with DSS (2.5 mM, 30 min) before immunoblotting for ASC oligomerization. (F) NLRP3 ATPase activity was measured using the ADP-Glo™ assay to quantify ATP-to-ADP conversion following TMH treatment. Data are presented as the mean ± SD (n = 3). Statistical analysis was performed using one-way ANOVA followed by Tukey’s multiple comparisons test. **P < 0.01, ***P < 0.001.

Article Snippet: Antibodies specific for human IL-1β (AF-401-NA) and mouse IL-1β (AF-201-NA) were purchased from R&D Systems (United States).

Techniques: Activation Assay, Activity Assay, Staining, Confocal Microscopy, Western Blot, Glo Assay

Toxicity assessment of TMH in zebrafish embryos. (A) Survival curves of zebrafish embryos treated with TMH at concentrations of 1, 10, or 100 μg/mL. Sixty embryos were used per condition and maintained in E3 medium. The control group was treated with DMSO (0.25%, v/v), corresponding to the highest TMH concentration. (B) Survival and phenotype distribution of 5 dpf embryos treated with TMH at distinct concentrations from 1 to 5 dpf. (C) Representative images showing developmental abnormalities observed in embryos treated with 10 μg/mL TMH at 5 dpf. (D) Representative images of Sudan Black B staining in 3 dpf embryos treated with vehicle control (0.0025% DMSO with PTU; upper panel) or TMH (1 μg/mL; lower panel). (E) Quantification of neutrophil counts in the CHT (red dashed outline) following treatment with TMH (1 μg/mL). Data are presented as mean ± SEM of individual embryos. Statistical significance was determined using an unpaired two-tailed Student’s t-test; n.s., not significant (p = 0.9997). Scale bars, 300 µm.

Journal: Frontiers in Pharmacology

Article Title: Thymelaea hirsuta (L.) Endl . extract attenuates NLRP3 inflammasome activation via modulation of ATPase activity

doi: 10.3389/fphar.2026.1781860

Figure Lengend Snippet: Toxicity assessment of TMH in zebrafish embryos. (A) Survival curves of zebrafish embryos treated with TMH at concentrations of 1, 10, or 100 μg/mL. Sixty embryos were used per condition and maintained in E3 medium. The control group was treated with DMSO (0.25%, v/v), corresponding to the highest TMH concentration. (B) Survival and phenotype distribution of 5 dpf embryos treated with TMH at distinct concentrations from 1 to 5 dpf. (C) Representative images showing developmental abnormalities observed in embryos treated with 10 μg/mL TMH at 5 dpf. (D) Representative images of Sudan Black B staining in 3 dpf embryos treated with vehicle control (0.0025% DMSO with PTU; upper panel) or TMH (1 μg/mL; lower panel). (E) Quantification of neutrophil counts in the CHT (red dashed outline) following treatment with TMH (1 μg/mL). Data are presented as mean ± SEM of individual embryos. Statistical significance was determined using an unpaired two-tailed Student’s t-test; n.s., not significant (p = 0.9997). Scale bars, 300 µm.

Article Snippet: Antibodies specific for human IL-1β (AF-401-NA) and mouse IL-1β (AF-201-NA) were purchased from R&D Systems (United States).

Techniques: Control, Concentration Assay, Staining, Two Tailed Test

TMH suppresses LPS-induced inflammatory cell recruitment in zebrafish embryos. (A) Representative images of neutrophil recruitment in the CHT in 3 dpf zebrafish embryos following LPS stimulation, assessed by Sudan Black B staining. Top panel: control embryos treated with 0.0025% DMSO (n = 29); middle panel: LPS-treated embryos (10 μg/mL; n = 32); bottom panel: embryos co-treated with LPS (10 μg/mL) and TMH (1 μg/mL; n = 33). (B) Quantification of neutrophil accumulation in the CHT following LPS stimulation with or without TMH treatment using Sudan Black B staining from (A) . (C) Representative images of whole-mount in situ hybridization showing mpx -positive neutrophils in 3 dpf embryos under LPS and TMH treatment conditions. Top panel (DMSO 0.0025%; n = 34); middle panel (LPS 10 μg/mL; n = 35); bottom panel (LPS 10 μg/mL with TMH 1 μg/mL; n = 39). (D) Quantification of mpx -positive cells within the CHT from (C) . (E) Representative confocal images of macrophages in 3 dpf Tg ( mpeg1 :EGFP) zebrafish embryos following LPS and TMH treatment. Top panel (DMSO 0.0025%; n = 8); middle panel (LPS 10 μg/mL; n = 11); bottom panel (LPS 10 μg/mL with TMH 1 μg/mL; n = 13). (F) Quantification of mpeg1 :EGFP-positive macrophages in the CHT region shown in (E) . Red dashed outline indicates the CHT. All data are presented as mean ± SEM. Statistical significance was determined using an unpaired two-tailed Student’s t-test. *P < 0.05; **P < 0.01; ***P < 0.05; ****P < 0.0001. Scale bars, 300 µm.

Journal: Frontiers in Pharmacology

Article Title: Thymelaea hirsuta (L.) Endl . extract attenuates NLRP3 inflammasome activation via modulation of ATPase activity

doi: 10.3389/fphar.2026.1781860

Figure Lengend Snippet: TMH suppresses LPS-induced inflammatory cell recruitment in zebrafish embryos. (A) Representative images of neutrophil recruitment in the CHT in 3 dpf zebrafish embryos following LPS stimulation, assessed by Sudan Black B staining. Top panel: control embryos treated with 0.0025% DMSO (n = 29); middle panel: LPS-treated embryos (10 μg/mL; n = 32); bottom panel: embryos co-treated with LPS (10 μg/mL) and TMH (1 μg/mL; n = 33). (B) Quantification of neutrophil accumulation in the CHT following LPS stimulation with or without TMH treatment using Sudan Black B staining from (A) . (C) Representative images of whole-mount in situ hybridization showing mpx -positive neutrophils in 3 dpf embryos under LPS and TMH treatment conditions. Top panel (DMSO 0.0025%; n = 34); middle panel (LPS 10 μg/mL; n = 35); bottom panel (LPS 10 μg/mL with TMH 1 μg/mL; n = 39). (D) Quantification of mpx -positive cells within the CHT from (C) . (E) Representative confocal images of macrophages in 3 dpf Tg ( mpeg1 :EGFP) zebrafish embryos following LPS and TMH treatment. Top panel (DMSO 0.0025%; n = 8); middle panel (LPS 10 μg/mL; n = 11); bottom panel (LPS 10 μg/mL with TMH 1 μg/mL; n = 13). (F) Quantification of mpeg1 :EGFP-positive macrophages in the CHT region shown in (E) . Red dashed outline indicates the CHT. All data are presented as mean ± SEM. Statistical significance was determined using an unpaired two-tailed Student’s t-test. *P < 0.05; **P < 0.01; ***P < 0.05; ****P < 0.0001. Scale bars, 300 µm.

Article Snippet: Antibodies specific for human IL-1β (AF-401-NA) and mouse IL-1β (AF-201-NA) were purchased from R&D Systems (United States).

Techniques: Staining, Control, In Situ Hybridization, Two Tailed Test

CTG12 inhibits NLRP3 inflammasome activation in mouse BMDMs and human THP1. A The structure of CTG12. B , C Cell viability of BMDMs ( B ) and THP1 cells ( C ) treated with CTG12. (D-H) Western blot analysis of IL-1β (p17), caspase-1 (p20) in culture supernatants (SN) and pro-IL-1β, caspase-1 (p45), NLRP3, ASC in whole cell lysates (WCL) of LPS-primed BMDMs treated with CTG12 and then stimulated with Nigericin (25 min) ( D ), supernatants were collected for the measurement of caspase-1( E ), IL-1β ( F ), LDH ( G ) and TNF-α ( H ). (I-M) THP-1 cells primed with PMA for 12 h were treated with CTG12 for 1 h and then stimulated with nigericin for 55 min. Western blot analysis of IL-1β (p17), caspase-1 (p20) in culture supernatants (SN) and pro-IL-1β, caspase-1 (p45), ASC in whole cell lysates (WCL) of THP-1 ( I ), supernatants were collected for the measurement of caspase-1( J ), IL-1β ( K ), LDH ( L ) and TNF-α ( M ). Coomassie blue-stained gels was used as loading control and Lamin B was used as a control for equal loading of the samples. Data represent as mean ± SEM ( n = 3). Compared to con, ** p < 0.01, **** p < 0.0001; compared to a concentration of 0 μM, # p < 0.05, ## p < 0.01, #### p < 0.0001 and ns: not significant (one-way ANOVA with Dunnett’s post-hoc test)

Journal: Cell Communication and Signaling : CCS

Article Title: Investigating the impact and mechanism of Licochalcone B derivative CTG12 on NLRP3 inflammasome

doi: 10.1186/s12964-026-02741-2

Figure Lengend Snippet: CTG12 inhibits NLRP3 inflammasome activation in mouse BMDMs and human THP1. A The structure of CTG12. B , C Cell viability of BMDMs ( B ) and THP1 cells ( C ) treated with CTG12. (D-H) Western blot analysis of IL-1β (p17), caspase-1 (p20) in culture supernatants (SN) and pro-IL-1β, caspase-1 (p45), NLRP3, ASC in whole cell lysates (WCL) of LPS-primed BMDMs treated with CTG12 and then stimulated with Nigericin (25 min) ( D ), supernatants were collected for the measurement of caspase-1( E ), IL-1β ( F ), LDH ( G ) and TNF-α ( H ). (I-M) THP-1 cells primed with PMA for 12 h were treated with CTG12 for 1 h and then stimulated with nigericin for 55 min. Western blot analysis of IL-1β (p17), caspase-1 (p20) in culture supernatants (SN) and pro-IL-1β, caspase-1 (p45), ASC in whole cell lysates (WCL) of THP-1 ( I ), supernatants were collected for the measurement of caspase-1( J ), IL-1β ( K ), LDH ( L ) and TNF-α ( M ). Coomassie blue-stained gels was used as loading control and Lamin B was used as a control for equal loading of the samples. Data represent as mean ± SEM ( n = 3). Compared to con, ** p < 0.01, **** p < 0.0001; compared to a concentration of 0 μM, # p < 0.05, ## p < 0.01, #### p < 0.0001 and ns: not significant (one-way ANOVA with Dunnett’s post-hoc test)

Article Snippet: Anti-human IL-1β (p17, 12242S), anti-Phospho-IRF3 (Ser396) (4947), caspase-1 antibody (4199S) and anti-ASC antibody (sc-22, 514-R) were obtained from Cell Signaling Technology (Germany).

Techniques: Activation Assay, Western Blot, Staining, Control, Concentration Assay

CTG12 specifically inhibits canonical and noncanonical NLRP3 inflammasome activation. A - C BMDMs were primed with LPS and then treated with CTG12 (5 μM), then stimulated with Nigericin, ATP, poly (I:C), or SiO₂. Western blot analysis of caspase-1 (p20) in culture supernatants (SN) and pro-IL-1β, pro-caspase-1 (p45), NLRP3 and ASC in whole-cell lysates (WCL); secretion of activated caspase-1 (p20) in the culture supernatant (SN) of BMDMs (A), supernatants were collected for the measurement of caspase-1 ( B ) and IL-1β ( C ). D - F BMDMs primed with Pam3CSK4 treated with CTG12 (5 μM), followed by cytosolic LPS. Western blot analysis of caspase-1 (p20) in culture supernatants (SN) and pro-IL-1β, pro-caspase-1 (p45), NLRP3 and ASC in whole-cell lysates (WCL); secretion of activated caspase-1 (p20) in the culture supernatant (SN) of BMDMs ( D ), supernatants were collected for the measurement of caspase-1 ( E ) and IL-1β ( F ). ( G - I ) BMDMs were primed with LPS treated with CTG12 (5 μM), then stimulated with Nigericin, Salmonella, poly (dA:dT). Western blot analysis of caspase-1 (p20) in culture supernatants (SN) and pro-IL-1β, pro-caspase-1 (p45), NLRP3 and ASC in whole-cell lysates (WCL); secretion of activated caspase-1 (p20) in the culture supernatant (SN) of BMDMs ( G ), supernatants were collected for the measurement of caspase-1 ( H ) and IL-1β ( I ). Coomassie blue-stained gels used as loading control and Lamin B used as a control for equal loading of the samples. Data represent as mean ± SEM ( n = 3). # p < 0.05, ## p < 0.01, ### p < 0.001, #### p < 0.0001 and ns: not significant (one-way ANOVA with Dunnett’s post-hoc test)

Journal: Cell Communication and Signaling : CCS

Article Title: Investigating the impact and mechanism of Licochalcone B derivative CTG12 on NLRP3 inflammasome

doi: 10.1186/s12964-026-02741-2

Figure Lengend Snippet: CTG12 specifically inhibits canonical and noncanonical NLRP3 inflammasome activation. A - C BMDMs were primed with LPS and then treated with CTG12 (5 μM), then stimulated with Nigericin, ATP, poly (I:C), or SiO₂. Western blot analysis of caspase-1 (p20) in culture supernatants (SN) and pro-IL-1β, pro-caspase-1 (p45), NLRP3 and ASC in whole-cell lysates (WCL); secretion of activated caspase-1 (p20) in the culture supernatant (SN) of BMDMs (A), supernatants were collected for the measurement of caspase-1 ( B ) and IL-1β ( C ). D - F BMDMs primed with Pam3CSK4 treated with CTG12 (5 μM), followed by cytosolic LPS. Western blot analysis of caspase-1 (p20) in culture supernatants (SN) and pro-IL-1β, pro-caspase-1 (p45), NLRP3 and ASC in whole-cell lysates (WCL); secretion of activated caspase-1 (p20) in the culture supernatant (SN) of BMDMs ( D ), supernatants were collected for the measurement of caspase-1 ( E ) and IL-1β ( F ). ( G - I ) BMDMs were primed with LPS treated with CTG12 (5 μM), then stimulated with Nigericin, Salmonella, poly (dA:dT). Western blot analysis of caspase-1 (p20) in culture supernatants (SN) and pro-IL-1β, pro-caspase-1 (p45), NLRP3 and ASC in whole-cell lysates (WCL); secretion of activated caspase-1 (p20) in the culture supernatant (SN) of BMDMs ( G ), supernatants were collected for the measurement of caspase-1 ( H ) and IL-1β ( I ). Coomassie blue-stained gels used as loading control and Lamin B used as a control for equal loading of the samples. Data represent as mean ± SEM ( n = 3). # p < 0.05, ## p < 0.01, ### p < 0.001, #### p < 0.0001 and ns: not significant (one-way ANOVA with Dunnett’s post-hoc test)

Techniques: Activation Assay, Western Blot, Staining, Control

CTG12 inhibits LPS-induced priming step of inflammasome activation and specifically inhibits canonical and noncanonical NLRP3 inflammasome activation by blocking NLRP3-dependent ASC oligomerization. A BMDMs were cultured with LPS for 4 h, then incubated with CTG12 for 1 h, or BMDMs were first treated with CTG12 for 1 h, followed by stimulation with LPS for 4 h, western blot analysis of protein levels of NLRP3, ASC, pro-IL-1β, Cas-1 p45, Lamin B. B BMDMs were primed with LPS treated with CTG12 (5 μM), then stimulated with Nigericin, western blot analysis of Triton X-insoluble microparticle cross-linking ASC. C BMDMs were primed with LPS treated with CTG12 (5 μM), then stimulated with Nigericin, ATP, poly(I:C), SiO 2 , western blot analysis of in Triton X insoluble microparticle cross-linked ASC. D BMDMs were primed with Pam3CSK4 treated with CTG12 (5 μM), followed by stimulation with ultra-LPS, western blot analysis of Triton X-insoluble microparticle cross-linking ASC. E BMDMs were primed with LPS treated with CTG12 (5 μM), then stimulated with Nigericin, salmonella or poly (dA:dT), western blot analysis of in Triton X insoluble microparticle cross-linked ASC. Coomassie blue-stained gels used as loading control and Lamin B used as a control for equal loading of the samples

Journal: Cell Communication and Signaling : CCS

Article Title: Investigating the impact and mechanism of Licochalcone B derivative CTG12 on NLRP3 inflammasome

doi: 10.1186/s12964-026-02741-2

Figure Lengend Snippet: CTG12 inhibits LPS-induced priming step of inflammasome activation and specifically inhibits canonical and noncanonical NLRP3 inflammasome activation by blocking NLRP3-dependent ASC oligomerization. A BMDMs were cultured with LPS for 4 h, then incubated with CTG12 for 1 h, or BMDMs were first treated with CTG12 for 1 h, followed by stimulation with LPS for 4 h, western blot analysis of protein levels of NLRP3, ASC, pro-IL-1β, Cas-1 p45, Lamin B. B BMDMs were primed with LPS treated with CTG12 (5 μM), then stimulated with Nigericin, western blot analysis of Triton X-insoluble microparticle cross-linking ASC. C BMDMs were primed with LPS treated with CTG12 (5 μM), then stimulated with Nigericin, ATP, poly(I:C), SiO 2 , western blot analysis of in Triton X insoluble microparticle cross-linked ASC. D BMDMs were primed with Pam3CSK4 treated with CTG12 (5 μM), followed by stimulation with ultra-LPS, western blot analysis of Triton X-insoluble microparticle cross-linking ASC. E BMDMs were primed with LPS treated with CTG12 (5 μM), then stimulated with Nigericin, salmonella or poly (dA:dT), western blot analysis of in Triton X insoluble microparticle cross-linked ASC. Coomassie blue-stained gels used as loading control and Lamin B used as a control for equal loading of the samples

Techniques: Activation Assay, Blocking Assay, Cell Culture, Incubation, Western Blot, Staining, Control

CTG12 alleviates LPS-induced acute systemic inflammation in mice. A - J Female mice (8 weeks) were injected intraperitoneally with CTG12 (0 mg/kg, 15 mg/kg, 30 mg/kg), MCC950 (40 mg/kg) or CTG12 (30 mg/kg) + MCC950 (40 mg/kg) for 1 h, followed by an injection of 20 mg/kg LPS for 5 h ( n = 6). The levels of IL-1β (A, B), IL-18 ( C , D ), IL-6 ( E , F ), TNF-α ( G , H ) and CXCL1/KC ( I , J ) in peritoneal lavage fluid and serum were analyzed by ELISA ( n = 6). Data represent as mean ± SD. Compared to con, **** p < 0.0001; compared to a concentration of 0 μM, # p < 0.05, ## p < 0.01, ### p < 0.001, #### p < 0.0001 and ns: not significant (one-way ANOVA with Dunnett’s post-hoc test)

Journal: Cell Communication and Signaling : CCS

Article Title: Investigating the impact and mechanism of Licochalcone B derivative CTG12 on NLRP3 inflammasome

doi: 10.1186/s12964-026-02741-2

Figure Lengend Snippet: CTG12 alleviates LPS-induced acute systemic inflammation in mice. A - J Female mice (8 weeks) were injected intraperitoneally with CTG12 (0 mg/kg, 15 mg/kg, 30 mg/kg), MCC950 (40 mg/kg) or CTG12 (30 mg/kg) + MCC950 (40 mg/kg) for 1 h, followed by an injection of 20 mg/kg LPS for 5 h ( n = 6). The levels of IL-1β (A, B), IL-18 ( C , D ), IL-6 ( E , F ), TNF-α ( G , H ) and CXCL1/KC ( I , J ) in peritoneal lavage fluid and serum were analyzed by ELISA ( n = 6). Data represent as mean ± SD. Compared to con, **** p < 0.0001; compared to a concentration of 0 μM, # p < 0.05, ## p < 0.01, ### p < 0.001, #### p < 0.0001 and ns: not significant (one-way ANOVA with Dunnett’s post-hoc test)

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

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