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ApexBio nlrp3 selective inhibitor mcc950
Nlrp3 Selective Inhibitor Mcc950, supplied by ApexBio, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/nlrp3+selective+inhibitor+mcc950/pm38811533-228-0-7?v=ApexBio
Average 90 stars, based on 1 article reviews

nlrp3 selective inhibitor mcc950 - by Bioz Stars, 2026-07

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The formation of the NLRP3 inflammasome induced the activation of ECs in the heart after dMCAO. (A) Western blotting shows the expression of NLRP3, ASC, and Casp-1 in vessels of the heart in the Sham and dMCAO animals. (B–D) Quantitative analysis of NLRP3, ASC, and Casp-1 levels relative to GAPDH. Each bar represents the mean ± SD. * p < 0.05 vs. Sham group ( n = 4 in each group). (E) Double-immunofluorescence staining of NLRP3 (green) with RECA-1 (red) in vessels of the heart in Sham or dMCAO 2 w rats injected with Veh or MCC950. Immunofluorescence staining of CD45 in the heart in Sham or dMCAO 2 w rats injected with Veh or MCC950. Scale bar: 25 μm. (F) The degree of overlap between NLRP3 and RECA-1 fluorescence based on the Pearson correlation coefficient in each group. (G) Quantitative analysis of CD45 + cells in each group. (H) Western blotting shows the expression of NLRP3, ASC, Casp-1, VCAM-1, ICAM-1, IL-1β, and TNF-α in vessels of the heart in the Sham and dMCAO rats injected with Veh or MCC950. (I–O) Quantitative analysis of NLRP3, ASC, Casp-1, VCAM-1, ICAM-1, IL-1β, and TNF-α levels relative to GAPDH. Each bar represents the mean ± SD. * p < 0.05 vs. Sham group, # p < 0.05 vs. dMCAO 2 w + Veh group ( n = 4 in each group). Sham, sham operation; dMCAO, distal middle cerebral artery occlusion; NLRP3, NOD-like receptor thermal protein domain associated protein 3; ASC, apoptosis-associated speck-like protein containing a CARD; Casp-1, caspase-1; Veh, Vehicle; RECA-1, rat endothelial cell antibody 1; VCAM-1, vascular cell adhesion molecule 1; ICAM-1, intercellular cell adhesion molecule-1; IL-1β, interleukin-1 beta; TNF-α, tumor necrosis factor-alpha; w, week.

Journal: Frontiers in Cardiovascular Medicine

Article Title: NF- κ B aggravates cardiac vascular endothelial injury by sustained activation of the NLRP3 inflammasome after ischemic stroke in rats

doi: 10.3389/fcvm.2026.1673693

Figure Lengend Snippet: The formation of the NLRP3 inflammasome induced the activation of ECs in the heart after dMCAO. (A) Western blotting shows the expression of NLRP3, ASC, and Casp-1 in vessels of the heart in the Sham and dMCAO animals. (B–D) Quantitative analysis of NLRP3, ASC, and Casp-1 levels relative to GAPDH. Each bar represents the mean ± SD. * p < 0.05 vs. Sham group ( n = 4 in each group). (E) Double-immunofluorescence staining of NLRP3 (green) with RECA-1 (red) in vessels of the heart in Sham or dMCAO 2 w rats injected with Veh or MCC950. Immunofluorescence staining of CD45 in the heart in Sham or dMCAO 2 w rats injected with Veh or MCC950. Scale bar: 25 μm. (F) The degree of overlap between NLRP3 and RECA-1 fluorescence based on the Pearson correlation coefficient in each group. (G) Quantitative analysis of CD45 + cells in each group. (H) Western blotting shows the expression of NLRP3, ASC, Casp-1, VCAM-1, ICAM-1, IL-1β, and TNF-α in vessels of the heart in the Sham and dMCAO rats injected with Veh or MCC950. (I–O) Quantitative analysis of NLRP3, ASC, Casp-1, VCAM-1, ICAM-1, IL-1β, and TNF-α levels relative to GAPDH. Each bar represents the mean ± SD. * p < 0.05 vs. Sham group, # p < 0.05 vs. dMCAO 2 w + Veh group ( n = 4 in each group). Sham, sham operation; dMCAO, distal middle cerebral artery occlusion; NLRP3, NOD-like receptor thermal protein domain associated protein 3; ASC, apoptosis-associated speck-like protein containing a CARD; Casp-1, caspase-1; Veh, Vehicle; RECA-1, rat endothelial cell antibody 1; VCAM-1, vascular cell adhesion molecule 1; ICAM-1, intercellular cell adhesion molecule-1; IL-1β, interleukin-1 beta; TNF-α, tumor necrosis factor-alpha; w, week.

Article Snippet: The NLRP3-selective inflammasome inhibitor MCC950 (MedChemExpress, HY-12815A), the NF- κ B p65 inhibitor PDTC (MedChemExpress, HY-18738), or the vehicle (normal saline, NS) was injected intraperitoneally 24 h before dMCAO.

Techniques: Activation Assay, Western Blot, Expressing, Double Immunofluorescence Staining, Injection, Immunofluorescence, Staining, Fluorescence

A , B, and F IF and TUNEL staining. Apoptotic cell nuclei were labeled with red fluorescence, all nuclei were stained with blue fluorescence, and TMEM119-positive cells were labeled with green fluorescence (magnification: ×40 and ×100). C and D Western blotting showed that Caspase1 and Gasdermin-D were activated after MCAO modeling. β-actin was used as a loading control. E Confocal microscopy revealed the colocalization of NLRP3 and ASC. NLRP3 was stained with red fluorescence, ASC was stained with purple fluorescence, TMEM119 was stained with green fluorescence, and nuclei were stained with blue fluorescence (magnification: ×40 and ×600). *** p < 0.001; **** p < 0.0001.

Journal: Cell Death Discovery

Article Title: HAX-1 interferes in assembly of NLRP3-ASC to block microglial pyroptosis in cerebral I/R injury

doi: 10.1038/s41420-024-02005-3

Figure Lengend Snippet: A , B, and F IF and TUNEL staining. Apoptotic cell nuclei were labeled with red fluorescence, all nuclei were stained with blue fluorescence, and TMEM119-positive cells were labeled with green fluorescence (magnification: ×40 and ×100). C and D Western blotting showed that Caspase1 and Gasdermin-D were activated after MCAO modeling. β-actin was used as a loading control. E Confocal microscopy revealed the colocalization of NLRP3 and ASC. NLRP3 was stained with red fluorescence, ASC was stained with purple fluorescence, TMEM119 was stained with green fluorescence, and nuclei were stained with blue fluorescence (magnification: ×40 and ×600). *** p < 0.001; **** p < 0.0001.

Article Snippet: To further investigate the effects of HAX-1 on pyroptosis, we used a selective NLRP3 inhibitor, MCC950(APExBIO), in the microglia to investigate the effects of HAX-1 on the pyroptosis pathway.

Techniques: TUNEL Assay, Staining, Labeling, Fluorescence, Western Blot, Control, Confocal Microscopy

A Western blotting indicated that HAX-1 expression decreased after OGD/R modeling. β-actin was used as a loading control. B – D Western blotting indicated that HAX-1 regulated the activation of Caspase1 and Gasdermin-D. β-actin was used as a loading control. E Confocal microscopy demonstrated the colocalization of NLRP3 and ASC. NLRP3 was stained with red fluorescence, and ASC was stained with green fluorescence (magnification: ×1000). * p < 0.05; ** p < 0.01, #### p < 0.0001.

Journal: Cell Death Discovery

Article Title: HAX-1 interferes in assembly of NLRP3-ASC to block microglial pyroptosis in cerebral I/R injury

doi: 10.1038/s41420-024-02005-3

Figure Lengend Snippet: A Western blotting indicated that HAX-1 expression decreased after OGD/R modeling. β-actin was used as a loading control. B – D Western blotting indicated that HAX-1 regulated the activation of Caspase1 and Gasdermin-D. β-actin was used as a loading control. E Confocal microscopy demonstrated the colocalization of NLRP3 and ASC. NLRP3 was stained with red fluorescence, and ASC was stained with green fluorescence (magnification: ×1000). * p < 0.05; ** p < 0.01, #### p < 0.0001.

Techniques: Western Blot, Expressing, Control, Activation Assay, Confocal Microscopy, Staining, Fluorescence

A – C Western blot showed the inhibition of NLRP3 blocked the effects of HAX-1 on the activation of Caspase1/Gasdermin D in microglia, β-actin was used as a loading control. D – F Co-immunoprecipitation (Co-IP) showed that HAX-1 affected the interaction between NLRP3 and ASC. G Confocal microscopy demonstrated the colocalization of HAX-1, NLRP3, and ASC. HAX-1 was stained with green fluorescence, NLRP3 was stained with red fluorescence, and ASC was stained with purple fluorescence (magnification: ×1000). * p < 0.05; ** p < 0.01, *** p < 0.001.

Journal: Cell Death Discovery

Article Title: HAX-1 interferes in assembly of NLRP3-ASC to block microglial pyroptosis in cerebral I/R injury

doi: 10.1038/s41420-024-02005-3

Figure Lengend Snippet: A – C Western blot showed the inhibition of NLRP3 blocked the effects of HAX-1 on the activation of Caspase1/Gasdermin D in microglia, β-actin was used as a loading control. D – F Co-immunoprecipitation (Co-IP) showed that HAX-1 affected the interaction between NLRP3 and ASC. G Confocal microscopy demonstrated the colocalization of HAX-1, NLRP3, and ASC. HAX-1 was stained with green fluorescence, NLRP3 was stained with red fluorescence, and ASC was stained with purple fluorescence (magnification: ×1000). * p < 0.05; ** p < 0.01, *** p < 0.001.

Techniques: Western Blot, Inhibition, Activation Assay, Control, Immunoprecipitation, Co-Immunoprecipitation Assay, Confocal Microscopy, Staining, Fluorescence

A – C Confocal microscopy revealed the colocalization of NLRP3, ASC, and Caspase1. Nuclei were stained with blue fluorescence, NLRP3 was stained with green fluorescence, ASC was stained with red fluorescence, and Caspase 1 was stained with purple fluorescence (original magnification: ×1000). D – F Co-immunoprecipitation (Co-IP) showed that HAX-1 affected the interaction between NLRP3 and ASC in tissue. * p < 0.05; ** p < 0.01, *** p < 0.001, **** p < 0.0001.

Journal: Cell Death Discovery

Article Title: HAX-1 interferes in assembly of NLRP3-ASC to block microglial pyroptosis in cerebral I/R injury

doi: 10.1038/s41420-024-02005-3

Figure Lengend Snippet: A – C Confocal microscopy revealed the colocalization of NLRP3, ASC, and Caspase1. Nuclei were stained with blue fluorescence, NLRP3 was stained with green fluorescence, ASC was stained with red fluorescence, and Caspase 1 was stained with purple fluorescence (original magnification: ×1000). D – F Co-immunoprecipitation (Co-IP) showed that HAX-1 affected the interaction between NLRP3 and ASC in tissue. * p < 0.05; ** p < 0.01, *** p < 0.001, **** p < 0.0001.

Techniques: Confocal Microscopy, Staining, Fluorescence, Immunoprecipitation, Co-Immunoprecipitation Assay

A – C BLI assay indicated the combination among HAX-1, ASC, NLRP3. D and E BLI assay tested the competitive binding of HAX-1 and ASC to NLRP3. F – H Molecular docking simulates NLRP3–ASC–HAX1 interaction. NLRP3 was labeled with red and HAX-1 was labeled with blue, ASC labeled with purple.

Journal: Cell Death Discovery

Article Title: HAX-1 interferes in assembly of NLRP3-ASC to block microglial pyroptosis in cerebral I/R injury

doi: 10.1038/s41420-024-02005-3

Figure Lengend Snippet: A – C BLI assay indicated the combination among HAX-1, ASC, NLRP3. D and E BLI assay tested the competitive binding of HAX-1 and ASC to NLRP3. F – H Molecular docking simulates NLRP3–ASC–HAX1 interaction. NLRP3 was labeled with red and HAX-1 was labeled with blue, ASC labeled with purple.

Techniques: Binding Assay, Labeling

Figure 1. Effects of silica-induced NLRP3 inflammasome activation on the disorganization of the LSPC-derived airway epithelium in the ALI model. (A) Representative photographs of immunohistochemistry for NLRP3, Caspase-1 and IL-1β staining in the z-stack of ALI cultures. Scale bar, 20 μm. (B) Representative images and western blot analysis of NLRP3, pro-Caspase-1, ASC and Caspase-1 p20 in ALI cultures. MCC950 markedly decreased silica-induced NLRP3 inflammasome activation in the LSPC-derived airway epithelium (n=3-4). Data are presented as the mean ± standard error of the mean (SEM): *P<0.05, **P<0.01, ***P<0.001. (C) Representative images of H&E, PAS and Masson’s trichrome staining in the z-stack of ALI cultures. Large cavities (H&E, black arrows), mucus overproduction (PAS, black arrows) and collagen fiber accumulation (Masson, black arrows). Scale bar, 20 μm. (D, E & F) MCC950 markedly reduced the thickness of silica-induced airway epithelium (D), area (E) and cell numbers (F) under high magnification (×400) (n=3). Data are expressed as the mean ± SEM: ****P<0.0001.

Journal: International journal of biological sciences

Article Title: NLRP3 Inflammasome Mediates Silica-induced Lung Epithelial Injury and Aberrant Regeneration in Lung Stem/Progenitor Cell-derived Organotypic Models.

doi: 10.7150/ijbs.80605

Figure Lengend Snippet: Figure 1. Effects of silica-induced NLRP3 inflammasome activation on the disorganization of the LSPC-derived airway epithelium in the ALI model. (A) Representative photographs of immunohistochemistry for NLRP3, Caspase-1 and IL-1β staining in the z-stack of ALI cultures. Scale bar, 20 μm. (B) Representative images and western blot analysis of NLRP3, pro-Caspase-1, ASC and Caspase-1 p20 in ALI cultures. MCC950 markedly decreased silica-induced NLRP3 inflammasome activation in the LSPC-derived airway epithelium (n=3-4). Data are presented as the mean ± standard error of the mean (SEM): *P<0.05, **P<0.01, ***P<0.001. (C) Representative images of H&E, PAS and Masson’s trichrome staining in the z-stack of ALI cultures. Large cavities (H&E, black arrows), mucus overproduction (PAS, black arrows) and collagen fiber accumulation (Masson, black arrows). Scale bar, 20 μm. (D, E & F) MCC950 markedly reduced the thickness of silica-induced airway epithelium (D), area (E) and cell numbers (F) under high magnification (×400) (n=3). Data are expressed as the mean ± SEM: ****P<0.0001.

Article Snippet: The NLRP3 inflammasome selective inhibitor MCC950 (CAS256373-96-3) was purchased from Selleck Chemicals and dissolved in sterile normal saline to prepare a 10 mM stock solution.

Techniques: Activation Assay, Derivative Assay, Immunohistochemistry, Staining, Western Blot

Figure 2. Effects of silica-induced NLRP3 inflammasome activation on pyroptosis of LSPC-derived airway epithelial cells in the ALI model. (A) Representative images and western blot analysis of GSDMD and GSDMD N-terminal domains in ALI cultures. MCC950 attenuated silica-induced pyroptosis with the downregulated expression of GSDMD and GSDMD N-terminal (n=5). Data are shown as the mean ± SEM: *P<0.05, **P<0.01, ***P<0.001. (B) Representative photographs of immunofluorescence staining for GSDMD in the z-stack of ALI cultures. White arrows indicate active GSDMD with an intense signal on the cell membrane. Scale bar, 50 μm.

Journal: International journal of biological sciences

Article Title: NLRP3 Inflammasome Mediates Silica-induced Lung Epithelial Injury and Aberrant Regeneration in Lung Stem/Progenitor Cell-derived Organotypic Models.

doi: 10.7150/ijbs.80605

Figure Lengend Snippet: Figure 2. Effects of silica-induced NLRP3 inflammasome activation on pyroptosis of LSPC-derived airway epithelial cells in the ALI model. (A) Representative images and western blot analysis of GSDMD and GSDMD N-terminal domains in ALI cultures. MCC950 attenuated silica-induced pyroptosis with the downregulated expression of GSDMD and GSDMD N-terminal (n=5). Data are shown as the mean ± SEM: *P<0.05, **P<0.01, ***P<0.001. (B) Representative photographs of immunofluorescence staining for GSDMD in the z-stack of ALI cultures. White arrows indicate active GSDMD with an intense signal on the cell membrane. Scale bar, 50 μm.

Article Snippet: The NLRP3 inflammasome selective inhibitor MCC950 (CAS256373-96-3) was purchased from Selleck Chemicals and dissolved in sterile normal saline to prepare a 10 mM stock solution.

Techniques: Activation Assay, Derivative Assay, Western Blot, Expressing, Immunofluorescence, Staining, Membrane

Figure 3. Effects of silica on mucociliary differentiation, multiciliogenesis and hypersecretion of the LSPC-derived airway epithelium in the ALI model. (A) Representative immunofluorescent images of ALI cultures in the z-stack. ACT (green): cilia marker, MUC5AC (red): mucus-producing goblet cell marker. Scale bar, 50 μm. (B) 3D reconstruction (xyz plane) of ACT (green) and MUC5AC (red) staining of ALI cultures. (C) MCC950 treatment decreased the percentage of ACT-positive or MUC5AC-positive stained area in the x-y plane of ALI cultures (n=3). Data are shown as the mean ± SEM: *P<0.05, **P<0.01, ****P<0.0001. (D) 3D reconstruction (xyz plane) of MUC5B (green) staining of ALI cultures.

Journal: International journal of biological sciences

Article Title: NLRP3 Inflammasome Mediates Silica-induced Lung Epithelial Injury and Aberrant Regeneration in Lung Stem/Progenitor Cell-derived Organotypic Models.

doi: 10.7150/ijbs.80605

Figure Lengend Snippet: Figure 3. Effects of silica on mucociliary differentiation, multiciliogenesis and hypersecretion of the LSPC-derived airway epithelium in the ALI model. (A) Representative immunofluorescent images of ALI cultures in the z-stack. ACT (green): cilia marker, MUC5AC (red): mucus-producing goblet cell marker. Scale bar, 50 μm. (B) 3D reconstruction (xyz plane) of ACT (green) and MUC5AC (red) staining of ALI cultures. (C) MCC950 treatment decreased the percentage of ACT-positive or MUC5AC-positive stained area in the x-y plane of ALI cultures (n=3). Data are shown as the mean ± SEM: *P<0.05, **P<0.01, ****P<0.0001. (D) 3D reconstruction (xyz plane) of MUC5B (green) staining of ALI cultures.

Article Snippet: The NLRP3 inflammasome selective inhibitor MCC950 (CAS256373-96-3) was purchased from Selleck Chemicals and dissolved in sterile normal saline to prepare a 10 mM stock solution.

Techniques: Derivative Assay, Marker, Staining

Figure 4. Effects of silica on ciliary dysplasia and dyskinesia in the LSPC-derived airway epithelium in the ALI model. (A) Collapsed and entangled cilia and mucus globules (red arrows) were observed on the apical surface of the airway epithelium in the silica-treated group by scanning electron microscopy (SEM). MCC950 treatment partially alleviated the silica-induced distortion of cilia architecture and accumulation of large mucus globules. Scale bars, 10 μm and 1 μm (magnified picture). (B) Transverse sections of cilia on the apical surface of the airway epithelium revealed that the normal ultrastructure of “9*2+2” microtubules was damaged in the silica-treated group according to transmission electron microscopy (TEM). MCC950 treatment partially ameliorated the fusion of silica-induced cilia with the plasma membrane. Scale bar, 200 nm. (C) Representative ROI count results obtained from the ciliaFA plugin in ImageJ. (D) Selective NLRP3 inflammasome inhibitor MCC950 improved silica-induced ciliary dyskinesia as determined by measuring the ciliary beat frequency (CBF) (n=3). Data are presented as the mean ± SEM: *P<0.05, **P<0.01.

Journal: International journal of biological sciences

Article Title: NLRP3 Inflammasome Mediates Silica-induced Lung Epithelial Injury and Aberrant Regeneration in Lung Stem/Progenitor Cell-derived Organotypic Models.

doi: 10.7150/ijbs.80605

Figure Lengend Snippet: Figure 4. Effects of silica on ciliary dysplasia and dyskinesia in the LSPC-derived airway epithelium in the ALI model. (A) Collapsed and entangled cilia and mucus globules (red arrows) were observed on the apical surface of the airway epithelium in the silica-treated group by scanning electron microscopy (SEM). MCC950 treatment partially alleviated the silica-induced distortion of cilia architecture and accumulation of large mucus globules. Scale bars, 10 μm and 1 μm (magnified picture). (B) Transverse sections of cilia on the apical surface of the airway epithelium revealed that the normal ultrastructure of “9*2+2” microtubules was damaged in the silica-treated group according to transmission electron microscopy (TEM). MCC950 treatment partially ameliorated the fusion of silica-induced cilia with the plasma membrane. Scale bar, 200 nm. (C) Representative ROI count results obtained from the ciliaFA plugin in ImageJ. (D) Selective NLRP3 inflammasome inhibitor MCC950 improved silica-induced ciliary dyskinesia as determined by measuring the ciliary beat frequency (CBF) (n=3). Data are presented as the mean ± SEM: *P<0.05, **P<0.01.

Article Snippet: The NLRP3 inflammasome selective inhibitor MCC950 (CAS256373-96-3) was purchased from Selleck Chemicals and dissolved in sterile normal saline to prepare a 10 mM stock solution.

Techniques: Derivative Assay, Electron Microscopy, Transmission Assay, Clinical Proteomics, Membrane

Figure 5. Effects of silica-induced NLRP3 inflammasome activation on cell proliferation and epithelial-mesenchymal transition (EMT) of the LSPC-derived airway epithelium in the ALI model. (A) Representative photographs of the EdU incorporation assay of ALI cultures in the x-y plane. Scale bar, 50 μm. (B) Quantification of EdU-positive cells in the x-y plane (n=3). The proportion of silica-induced EdU-positive cells was decreased by the NLRP3 inflammasome inhibitor MCC950. Data are presented as the mean ± SEM: ****P<0.0001. (C) Representative images of positive immunostaining of ZO-1 (red) and Vimentin (green) in the x-y plane. Scale bar, 50 μm. (D) Representative photographs and western blot analysis of epithelial markers (ZO-1 and E-Cadherin) and a mesenchymal marker (Vimentin) in ALI cultures. MCC950 treatment alleviated silica-induced EMT with upregulation of ZO-1 (n=4) and E-Cadherin (n=3) and downregulation of Vimentin (n=5). The data are expressed as the mean ± SEM: *P<0.05, **P<0.01.

Journal: International journal of biological sciences

Article Title: NLRP3 Inflammasome Mediates Silica-induced Lung Epithelial Injury and Aberrant Regeneration in Lung Stem/Progenitor Cell-derived Organotypic Models.

doi: 10.7150/ijbs.80605

Figure Lengend Snippet: Figure 5. Effects of silica-induced NLRP3 inflammasome activation on cell proliferation and epithelial-mesenchymal transition (EMT) of the LSPC-derived airway epithelium in the ALI model. (A) Representative photographs of the EdU incorporation assay of ALI cultures in the x-y plane. Scale bar, 50 μm. (B) Quantification of EdU-positive cells in the x-y plane (n=3). The proportion of silica-induced EdU-positive cells was decreased by the NLRP3 inflammasome inhibitor MCC950. Data are presented as the mean ± SEM: ****P<0.0001. (C) Representative images of positive immunostaining of ZO-1 (red) and Vimentin (green) in the x-y plane. Scale bar, 50 μm. (D) Representative photographs and western blot analysis of epithelial markers (ZO-1 and E-Cadherin) and a mesenchymal marker (Vimentin) in ALI cultures. MCC950 treatment alleviated silica-induced EMT with upregulation of ZO-1 (n=4) and E-Cadherin (n=3) and downregulation of Vimentin (n=5). The data are expressed as the mean ± SEM: *P<0.05, **P<0.01.

Article Snippet: The NLRP3 inflammasome selective inhibitor MCC950 (CAS256373-96-3) was purchased from Selleck Chemicals and dissolved in sterile normal saline to prepare a 10 mM stock solution.

Techniques: Activation Assay, Derivative Assay, Immunostaining, Western Blot, Marker

Figure 6. Effects of silica-induced NLRP3 inflammasome activation on basal cell ectopic distribution and SOX2/SOX9 high expression in the ALI model. (A) Representative images of immunofluorescence staining for p63 (red) and NGFR (green) in the z-stack of ALI cultures. The selected region (white box) indicated the silica-induced ectopic distribution of airway epithelial basal cells in the ALI model. Scale bar, 50 μm. (B) Representative images of immunofluorescence staining for p63 (red) and SOX2 (green) in the z-stack of ALI cultures. The white arrows indicate the silica-induced ectopic distribution of SOX2+ basal cells in ALI cultures. Scale bar, 50 μm. (C) Quantification of SOX2+ basal cells in the z-stack of ALI cultures (n=3). The percentage of SOX2+ basal cells in the silica-treated group was decreased by MCC950. The data are presented as the mean ± SEM: **P<0.01, ***P<0.001. (D) Representative images of immunofluorescence staining for SOX9 (red) and SOX2 (green) in the z-stack of ALI cultures. The white arrows indicate silica-induced SOX9/SOX2 double-positive cells in the ALI model. Scale bar, 50 μm. (E) Quantification of SOX9/SOX2 double-positive cells in the z-stack of ALI cultures (n=3). The percentage of double-positive cells in the silica-treated group was reduced by MCC950. The data are presented as the mean ± SEM: ***P<0.001, ****P<0.0001. (F, G & H) Representative photographs and western blot analysis of p63 (F), SOX9 (G) and SOX2 (H) in ALI cultures. MCC950 markedly reduced silica-induced increases in the protein levels of p63 (n=5) and SOX9 (n=3), while no significant differences in SOX2 levels (n=3) were observed. The data are expressed as the mean ± SEM: *P<0.05, **P<0.01, ***P<0.001.

Journal: International journal of biological sciences

Article Title: NLRP3 Inflammasome Mediates Silica-induced Lung Epithelial Injury and Aberrant Regeneration in Lung Stem/Progenitor Cell-derived Organotypic Models.

doi: 10.7150/ijbs.80605

Figure Lengend Snippet: Figure 6. Effects of silica-induced NLRP3 inflammasome activation on basal cell ectopic distribution and SOX2/SOX9 high expression in the ALI model. (A) Representative images of immunofluorescence staining for p63 (red) and NGFR (green) in the z-stack of ALI cultures. The selected region (white box) indicated the silica-induced ectopic distribution of airway epithelial basal cells in the ALI model. Scale bar, 50 μm. (B) Representative images of immunofluorescence staining for p63 (red) and SOX2 (green) in the z-stack of ALI cultures. The white arrows indicate the silica-induced ectopic distribution of SOX2+ basal cells in ALI cultures. Scale bar, 50 μm. (C) Quantification of SOX2+ basal cells in the z-stack of ALI cultures (n=3). The percentage of SOX2+ basal cells in the silica-treated group was decreased by MCC950. The data are presented as the mean ± SEM: **P<0.01, ***P<0.001. (D) Representative images of immunofluorescence staining for SOX9 (red) and SOX2 (green) in the z-stack of ALI cultures. The white arrows indicate silica-induced SOX9/SOX2 double-positive cells in the ALI model. Scale bar, 50 μm. (E) Quantification of SOX9/SOX2 double-positive cells in the z-stack of ALI cultures (n=3). The percentage of double-positive cells in the silica-treated group was reduced by MCC950. The data are presented as the mean ± SEM: ***P<0.001, ****P<0.0001. (F, G & H) Representative photographs and western blot analysis of p63 (F), SOX9 (G) and SOX2 (H) in ALI cultures. MCC950 markedly reduced silica-induced increases in the protein levels of p63 (n=5) and SOX9 (n=3), while no significant differences in SOX2 levels (n=3) were observed. The data are expressed as the mean ± SEM: *P<0.05, **P<0.01, ***P<0.001.

Article Snippet: The NLRP3 inflammasome selective inhibitor MCC950 (CAS256373-96-3) was purchased from Selleck Chemicals and dissolved in sterile normal saline to prepare a 10 mM stock solution.

Techniques: Activation Assay, Expressing, Immunofluorescence, Staining, Western Blot

Figure 7. Effects of silica-induced NLRP3 inflammasome activation on the NF-κB, Shh-Gli and Wnt/β-catenin pathways in ALI culture. (A) Western blot analysis revealed that the phosphorylation-activation of IκBα (n=5) and NF-κB p65 (n=4) induced by silica was reversed by MCC950. Data are expressed as the mean ± SEM: ***P<0.001, ****P<0.0001. (B) Western blot analysis showed that the increased expression of Shh-Gli pathway-related proteins Shh (n=4), Smo (n=3) and Gli1 (n=3) induced by silica could be reversed by MCC950. The data are presented as the mean ± SEM: *P<0.05, **P<0.01, ****P<0.0001. (C) The high expression of Wnt10a (n=4) in the silica-treated group was measured by western blot and was reduced by MCC950. The data are expressed as the mean ± SEM: **P<0.01, ***P<0.001. (D) Western blot results showed that the silica-induced increased expression of the canonical Wnt/β-catenin signaling pathway-related molecules phosphorylated GSK-3β (n=3) and β-catenin (n=5) was reversed by MCC950. The data are presented as the mean ± SEM: **P<0.01, ****P<0.0001.

Journal: International journal of biological sciences

Article Title: NLRP3 Inflammasome Mediates Silica-induced Lung Epithelial Injury and Aberrant Regeneration in Lung Stem/Progenitor Cell-derived Organotypic Models.

doi: 10.7150/ijbs.80605

Figure Lengend Snippet: Figure 7. Effects of silica-induced NLRP3 inflammasome activation on the NF-κB, Shh-Gli and Wnt/β-catenin pathways in ALI culture. (A) Western blot analysis revealed that the phosphorylation-activation of IκBα (n=5) and NF-κB p65 (n=4) induced by silica was reversed by MCC950. Data are expressed as the mean ± SEM: ***P<0.001, ****P<0.0001. (B) Western blot analysis showed that the increased expression of Shh-Gli pathway-related proteins Shh (n=4), Smo (n=3) and Gli1 (n=3) induced by silica could be reversed by MCC950. The data are presented as the mean ± SEM: *P<0.05, **P<0.01, ****P<0.0001. (C) The high expression of Wnt10a (n=4) in the silica-treated group was measured by western blot and was reduced by MCC950. The data are expressed as the mean ± SEM: **P<0.01, ***P<0.001. (D) Western blot results showed that the silica-induced increased expression of the canonical Wnt/β-catenin signaling pathway-related molecules phosphorylated GSK-3β (n=3) and β-catenin (n=5) was reversed by MCC950. The data are presented as the mean ± SEM: **P<0.01, ****P<0.0001.

Article Snippet: The NLRP3 inflammasome selective inhibitor MCC950 (CAS256373-96-3) was purchased from Selleck Chemicals and dissolved in sterile normal saline to prepare a 10 mM stock solution.

Techniques: Activation Assay, Western Blot, Phospho-proteomics, Expressing

Figure 8. Effects of silica-induced NLRP3 inflammasome activation on lung organoid development in 3D culture. (A) Representative photographs of the immunohistochemistry for IL-1β staining of lung organoids. Scale bar, 20 μm. (B) Representative photographs of immunofluorescence staining for ASC specks in lung organoids. The white arrows indicate silica-induced ASC speck formation in the 3D system. Scale bar, 50 μm. (C) Representative images of immunofluorescence staining for GSDMD in organoids. The white arrows indicate the signal intensity of active GSDMD on the cell membrane in the silica-treated group. Scale bar, 50 μm. (D) Representative images of the lung organoids and quantification of the organoid area (n=3). Silica inhibited lung organoid development in the 3D culture, which was improved by MCC950 treatment. Scale bar, 100 μm. The data are presented as the mean ± SEM: ****P<0.0001. (E, F, G & H) Representative photographs of immunofluorescence staining for MUC5AC and ACT (E), Ki67 (F), p63 and SOX2 (G), SOX9 and SOX2 (H) in the lung organoids. Scale bar, 50 μm. (I & J) Quantification of p63/SOX2 (I) and SOX9/SOX2 (J) double-positive cell numbers in the organoids (n=3). The data are expressed as the mean ± SEM: **P<0.01, ****P<0.0001.

Journal: International journal of biological sciences

Article Title: NLRP3 Inflammasome Mediates Silica-induced Lung Epithelial Injury and Aberrant Regeneration in Lung Stem/Progenitor Cell-derived Organotypic Models.

doi: 10.7150/ijbs.80605

Figure Lengend Snippet: Figure 8. Effects of silica-induced NLRP3 inflammasome activation on lung organoid development in 3D culture. (A) Representative photographs of the immunohistochemistry for IL-1β staining of lung organoids. Scale bar, 20 μm. (B) Representative photographs of immunofluorescence staining for ASC specks in lung organoids. The white arrows indicate silica-induced ASC speck formation in the 3D system. Scale bar, 50 μm. (C) Representative images of immunofluorescence staining for GSDMD in organoids. The white arrows indicate the signal intensity of active GSDMD on the cell membrane in the silica-treated group. Scale bar, 50 μm. (D) Representative images of the lung organoids and quantification of the organoid area (n=3). Silica inhibited lung organoid development in the 3D culture, which was improved by MCC950 treatment. Scale bar, 100 μm. The data are presented as the mean ± SEM: ****P<0.0001. (E, F, G & H) Representative photographs of immunofluorescence staining for MUC5AC and ACT (E), Ki67 (F), p63 and SOX2 (G), SOX9 and SOX2 (H) in the lung organoids. Scale bar, 50 μm. (I & J) Quantification of p63/SOX2 (I) and SOX9/SOX2 (J) double-positive cell numbers in the organoids (n=3). The data are expressed as the mean ± SEM: **P<0.01, ****P<0.0001.

Article Snippet: The NLRP3 inflammasome selective inhibitor MCC950 (CAS256373-96-3) was purchased from Selleck Chemicals and dissolved in sterile normal saline to prepare a 10 mM stock solution.

Techniques: Activation Assay, Immunohistochemistry, Staining, Immunofluorescence, Membrane

Figure 7. Inhibition of IL-1β by MCC950 ameliorates the severity of colitis challenged with C. difficile. (a) Schematic diagram of the MCC950 inhibition model. After DSS mice were challenged with C. difficile on day 7, they were injected i.P. with MCC950 at a dose of 20 mg/kg/mouse on days 7 and 8, and PBS was used as a negative control. (b – d) Disease severity was assessed by weight loss (b), H&E staining (c), and histological sores (d). (e and f) Expression of IL-1β, IL-6, and CXCL2 mRNA in colonic tissue (e) and CXCL2 mRNA in

Journal: Gut microbes

Article Title: Clostridioides difficile aggravates dextran sulfate solution (DSS)-induced colitis by shaping the gut microbiota and promoting neutrophil recruitment.

doi: 10.1080/19490976.2023.2192478

Figure Lengend Snippet: Figure 7. Inhibition of IL-1β by MCC950 ameliorates the severity of colitis challenged with C. difficile. (a) Schematic diagram of the MCC950 inhibition model. After DSS mice were challenged with C. difficile on day 7, they were injected i.P. with MCC950 at a dose of 20 mg/kg/mouse on days 7 and 8, and PBS was used as a negative control. (b – d) Disease severity was assessed by weight loss (b), H&E staining (c), and histological sores (d). (e and f) Expression of IL-1β, IL-6, and CXCL2 mRNA in colonic tissue (e) and CXCL2 mRNA in

Article Snippet: To perform CXCR2 and NLRP3 inhibition in the in vivo model, the DSSCD group were administered the CXCR2 selective inhibitor SB225002 (Sigma Aldrich, USA) (1 mg/kg/mouse) or the NLRP3 selective inhibitor MCC950 (Selleck, USA) (20 mg/kg/mouse) intraperitoneally (i.p.) on days 7 and 8 (Figures 6a and 7a).

Techniques: Inhibition, Injection, Negative Control, Staining, Expressing

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