Journal: International Dental Journal

Article Title: Chemerin Promotes Oral Squamous Cell Carcinoma Progression via NLRP3-Mediated Pyroptosis and the GSDMD-N Pathway

doi: 10.1016/j.identj.2026.109541

Figure Lengend Snippet: Expression of chemerin and NLRP3 in OSCC. A, The results indicated that NLRP3 was highly expressed in the high-expression region of chemerin. B, Immunofluorescence double staining showed that chemerin (488 nm) and NLRP3 (650 nm) could be coexpressed and localised in OSCC cells (red for chemerin and green for NLRP3). C, Chemerin overexpression led to the increased expression of pyroptosis-related proteins, and vice versa. When the NLRP3 inhibitor (MCC950) was added to each group, the expression level of pyroptosis-related proteins was decreased. GAPDH was used as a control.

Article Snippet: The NLRP3 inhibitor (MCC950) was purchased from MCE (Item No. CSN18163 ).

Techniques: Expressing, Immunofluorescence, Double Staining, Over Expression, Control

Journal: International Dental Journal

Article Title: Chemerin Promotes Oral Squamous Cell Carcinoma Progression via NLRP3-Mediated Pyroptosis and the GSDMD-N Pathway

doi: 10.1016/j.identj.2026.109541

Figure Lengend Snippet: Chemerin promotes OSCC EMT through pyroptosis. The expression of EMT-related molecules was measured in Cal27 and SCC15 cell lines. After chemerin overexpression, the expression level of N-cadherin and vimentin was increased, and the expression level of E-cadherin was decreased. After MCC950 was added, the expression level of N-cadherin and vimentin was still decreased, whereas the expression level of E-cadherin was increased. Tubulin was used as the control.

Article Snippet: The NLRP3 inhibitor (MCC950) was purchased from MCE (Item No. CSN18163 ).

Techniques: Expressing, Over Expression, Control

Journal: International Dental Journal

Article Title: Chemerin Promotes Oral Squamous Cell Carcinoma Progression via NLRP3-Mediated Pyroptosis and the GSDMD-N Pathway

doi: 10.1016/j.identj.2026.109541

Figure Lengend Snippet: Chemerin promotes cell migration and invasion through pyroptosis. A, Transwell migration and invasion experiments showed that the proliferation and migration of OSCC cells were enhanced after chemerin overexpression. After MCC950 was added, the proliferation and migration abilities of cells were weakened. B, Scratch healing experiments showed that OSCC cell migration was enhanced after chemerin overexpression. After adding MCC950, the cell migration ability was weakened.

Article Snippet: The NLRP3 inhibitor (MCC950) was purchased from MCE (Item No. CSN18163 ).

Techniques: Migration, Over Expression

Journal: International Dental Journal

Article Title: Chemerin Promotes Oral Squamous Cell Carcinoma Progression via NLRP3-Mediated Pyroptosis and the GSDMD-N Pathway

doi: 10.1016/j.identj.2026.109541

Figure Lengend Snippet: Chemerin promotes cell proliferation through pyroptosis. A, The CCK-8 experiment showed that the OD value of OSCC cells increased after the overexpression of chemerin. The OD value decreases after chemerin knockdown. After MCC950 was added, the OD value of the OSCC cells decreased. B, Flow cytometry results indicated that in the GSDMD-N expression group, the proportion of OSCC cells entering the S phase increased, and cell proliferation was promoted. The knockdown group enriched for S-phase cells and inhibited cell proliferation. C, In the group with high GSDMD-N expression level, the expression level of cyclinE1 and cyclinD1 increased, and after adding MCC950, the expression level of cyclinE1 and cyclinD1 decreased. GAPDH was used as the control.

Article Snippet: The NLRP3 inhibitor (MCC950) was purchased from MCE (Item No. CSN18163 ).

Techniques: CCK-8 Assay, Over Expression, Knockdown, Flow Cytometry, Expressing, Control

Journal: International Dental Journal

Article Title: Chemerin Promotes Oral Squamous Cell Carcinoma Progression via NLRP3-Mediated Pyroptosis and the GSDMD-N Pathway

doi: 10.1016/j.identj.2026.109541

Figure Lengend Snippet: Effect of chemerin on the formation of subcutaneous tumours in nude mice. A, The results of tumour transplantation in nude mice indicated that the tumours in the CAL27-Chemerin group were larger and heavier than those in the Cal27 group ( P < .05). The tumours in the SCC15 group were larger and heavier than those in the SCC15-Chemerin-shRNA group ( P < .05). B, The immunohistochemical results indicated that the expression level of pyroptosis-related molecules (GSDMD and IL-1β) and NLRP3 was higher in the chemerin overexpression group and lower in the chemerin knockdown group.

Article Snippet: The NLRP3 inhibitor (MCC950) was purchased from MCE (Item No. CSN18163 ).

Techniques: Transplantation Assay, shRNA, Immunohistochemical staining, Expressing, Over Expression, Knockdown

Journal: European Journal of Immunology

Article Title: SYK Signalling in NLRP3 Inflammasome‐Mediated Response of Murine Microglia Activated by Immune Complexes Formed of Viral Proteins and Specific IgG

doi: 10.1002/eji.70199

Figure Lengend Snippet: The impact of SYK inhibition on NLRP3 activation. Cells were treated with VLPs (20 µg/mL) and mAbs (7.5 µg/mL) for 24 h, and 1 µM of SYK inhibitor R406 or NLRP3 inhibitor MCC950 was added 1 h before treatment. (A) Western blot data show the expression of the indicated protein in microglia lysates, and the images are representative of five to six experiments. (B) Quantification of NLRP3 expression from Western blot data, normalised to a loading control, N = 5–6. (C) Quantification of ASC speck formation in primary microglia, N = 6. (D, E) IL‐1β secretion and (F) TNF‐α secretion were tested by ELISA in microglia supernatants, (D) N = 4, (E) N = 4–6, (F) N = 8–9. (G) Fluorescent microscopy images of the immunostained NLRP3 (cyan) and ASC specks (yellow), NLRP3 was stained with primary Ab anti‐NLRP and secondary Ab—AlexaFluor 488, ASC specks were stained with primary Ab anti‐ASC‐PE. Representative images are shown. The scale bars indicate 50 µm in large images and 20 µm in magnified images. In (B–F), data are represented using a box plot with dots showing the number of individual experiments. Significance was established using one‐way ANOVA followed by Tukey's test * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

Article Snippet: SYK kinase inhibitor R406 (#inh‐r406), NLRP3 inhibitor MCC950 (#inh‐mcc), and Zymosan (#tlrl‐zyn) were from Invivogen.

Techniques: Inhibition, Activation Assay, Western Blot, Expressing, Control, Enzyme-linked Immunosorbent Assay, Microscopy, Staining

Journal: International Journal of Molecular Medicine

Article Title: Hypothermic machine perfusion protects DCD graft liver from ischemia-reperfusion injury by enhancing macrophage efferocytosis via KLF2-NLRP3 signaling

doi: 10.3892/ijmm.2026.5756

Figure Lengend Snippet: KLF2 inhibits the NLRP3-mediated pyroptosis pathway during CS/Rep in ECs. (A) Heatmap and (B) volcano plot of differentially expressed genes between control and ov-KLF2 HUVECs after CS/Rep treatment. mRNA levels of (C) KLF2 and (D) NLRP3 in ov-control and ov-KLF2 group of HUVECs following CS/Rep treatment were quantified using reverse transcription-quantitative PCR. (E) Co-IP analysis of the interaction between KLF2 and NLRP3. (F) Microstructure of HUVECS. (G) Representative Western blot images for KLF2, NLRP3, GSDMD, Caspase-1 and IL-18 in CS/Rep HUVECs. Quantitative analysis of KLF2 (H), NLRP3 (I), GSDMD (J), Caspase-1 (K) and IL-18 (L) protein expression based on western blot results from HUVECS of ov-control and ov-KLF2 groups. Quantitative analysis of KLF2 (M), NLRP3 (N), GSDMD (O), Caspase-1 (P) and IL-18 (Q) protein expression based on western blot results from HUVECS of sh-control and sh-KLF2 groups. (n=3). * P<0.05, ** P<0.01, *** P<0.001. KLF2, Kruppel-like Factor 2; CS/Rep, cold storage/reperfusion; HUVEC, human umbilical vein endothelial cells; ov, overexpression; IP, immunoprecipitation; GSDMD, gasdermin D; sh, short hairpin;; FC, fold-change.

Article Snippet: The incubation period between transfection and subsequent treatment was 72 h. To verify whether NLRP3 inhibition rescues the phenotypes resulting from KLF2 deficiency, sh-KLF2-transfected cells were treated (37°C) with 10 μ M NLRP3 inhibitor MCC950 (cat. no. HY12815, MedChemExpress) for 24 h and subjected to CS/Rep as aforementioned.

Techniques: Control, Reverse Transcription, Real-time Polymerase Chain Reaction, Co-Immunoprecipitation Assay, Western Blot, Expressing, Over Expression, Immunoprecipitation

Journal: medRxiv

Article Title: Airborne particulate matter enhances with monosodium urate crystals the secretion of IL-1β by human immune cells

doi: 10.64898/2026.02.26.26347218

Figure Lengend Snippet: Innate immune cell phenotype and IL-1 β expression after exposure of animals to CB+O 3 . Absolute counts for A) lavage neutrophils B) macrophages and C) particle-containing macrophages in lavage, n=4-6 per experiment. Evidence of NLRP3-inflammasome activation in the lungs after MSU injection and air pollution exposure day 8 post MSUc injection (D) pro-IL-1□ mRNA expression and E) IL-1□ concentration in lung lavage fluid, n=4-6 per experiment. * P <0.05, ** P <0.005, **** P <0.00005.

Article Snippet: NLRP3-inflammasome inhibitor MCC950 was purchased from Invivogen and used at 2 nmol/l.

Techniques: Expressing, Activation Assay, Injection, Concentration Assay

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