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nlrp3  (Bioss)


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    Bioss nlrp3
    Expression of chemerin and <t>NLRP3</t> 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.
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    Images

    1) Product Images from "Chemerin Promotes Oral Squamous Cell Carcinoma Progression via NLRP3-Mediated Pyroptosis and the GSDMD-N Pathway"

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

    Journal: International Dental Journal

    doi: 10.1016/j.identj.2026.109541

    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.
    Figure Legend 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.

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

    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.
    Figure Legend 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.

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



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    Expression of chemerin and <t>NLRP3</t> 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.
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    Expression of chemerin and <t>NLRP3</t> 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 <t>(MCC950)</t> was added to each group, the expression level of pyroptosis-related proteins was decreased. GAPDH was used as a control.
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    Expression of chemerin and <t>NLRP3</t> 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 <t>(MCC950)</t> was added to each group, the expression level of pyroptosis-related proteins was decreased. GAPDH was used as a control.
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    Propranolol suppressed <t>NLRP3</t> inflammasome activation in tMCAO mice (A) Western blot analysis of IBA-1, NLRP3, and IL-1β in the ischemic penumbra of different groups. (B–D) Quantitative analysis of IBA-1, NLRP3, and IL-1β expression ( n = 3 biological replicates per group, each with 3 technical replicates). Data were expressed as mean ± SD. Statistical analysis was performed using one-way ANOVA followed by Tukey’s post hoc test. ∗∗ p < 0.01 and ∗∗∗ p < 0.001 versus the Sham-operated group; # p < 0.05 versus the tMCAO group. (E) Immunofluorescence staining for NLRP3 of brain sections in the indicated groups. Scale bars, 100 μm (main image) and 30 μm (magnified view). (F) Quantitative analysis of NLRP3 positive cells ( n = 3 biological replicates per group, each with 3 technical replicates). Data were expressed as mean ± SD. Statistical analysis was performed using one-way ANOVA followed by Tukey’s post hoc test. ∗∗∗ p < 0.001 versus the Sham-operated group; # p < 0.05 versus the tMCAO group. (G) Immunofluorescence staining for IBA-1 of brain sections in the indicated groups. Scale bars, 50 μm (main image) and 10 μm (magnified view). (H) Representative images of microglia and heat maps of Sholl analysis were shown. Scale bar, 10 μm. (I) Sholl profile shows the number of intersections at different distances from the microglial soma in the indicated groups ( n = 4 biological replicates per group, each with 3 technical replicates). Data were expressed as mean ± SD. Statistical analysis was performed using two-way ANOVA followed by Tukey’s post hoc test. ∗∗∗∗ p < 0.0001 versus the Sham-operated group; #### p < 0.0001 versus the tMCAO group. (J and K) Quantitative analysis of process length (J) and endpoints (K) per cell ( n = 4 biological replicates per group, each with 3 technical replicates). Data were expressed as mean ± SD. Statistical analysis was performed using one-way ANOVA followed by Tukey’s post hoc test. ∗∗∗ p < 0.001 versus the Sham-operated group; # p < 0.05and ## p < 0.01 versus the tMCAO group.
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    Propranolol suppressed <t>NLRP3</t> inflammasome activation in tMCAO mice (A) Western blot analysis of IBA-1, NLRP3, and IL-1β in the ischemic penumbra of different groups. (B–D) Quantitative analysis of IBA-1, NLRP3, and IL-1β expression ( n = 3 biological replicates per group, each with 3 technical replicates). Data were expressed as mean ± SD. Statistical analysis was performed using one-way ANOVA followed by Tukey’s post hoc test. ∗∗ p < 0.01 and ∗∗∗ p < 0.001 versus the Sham-operated group; # p < 0.05 versus the tMCAO group. (E) Immunofluorescence staining for NLRP3 of brain sections in the indicated groups. Scale bars, 100 μm (main image) and 30 μm (magnified view). (F) Quantitative analysis of NLRP3 positive cells ( n = 3 biological replicates per group, each with 3 technical replicates). Data were expressed as mean ± SD. Statistical analysis was performed using one-way ANOVA followed by Tukey’s post hoc test. ∗∗∗ p < 0.001 versus the Sham-operated group; # p < 0.05 versus the tMCAO group. (G) Immunofluorescence staining for IBA-1 of brain sections in the indicated groups. Scale bars, 50 μm (main image) and 10 μm (magnified view). (H) Representative images of microglia and heat maps of Sholl analysis were shown. Scale bar, 10 μm. (I) Sholl profile shows the number of intersections at different distances from the microglial soma in the indicated groups ( n = 4 biological replicates per group, each with 3 technical replicates). Data were expressed as mean ± SD. Statistical analysis was performed using two-way ANOVA followed by Tukey’s post hoc test. ∗∗∗∗ p < 0.0001 versus the Sham-operated group; #### p < 0.0001 versus the tMCAO group. (J and K) Quantitative analysis of process length (J) and endpoints (K) per cell ( n = 4 biological replicates per group, each with 3 technical replicates). Data were expressed as mean ± SD. Statistical analysis was performed using one-way ANOVA followed by Tukey’s post hoc test. ∗∗∗ p < 0.001 versus the Sham-operated group; # p < 0.05and ## p < 0.01 versus the tMCAO group.
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    Propranolol suppressed <t>NLRP3</t> inflammasome activation in tMCAO mice (A) Western blot analysis of IBA-1, NLRP3, and IL-1β in the ischemic penumbra of different groups. (B–D) Quantitative analysis of IBA-1, NLRP3, and IL-1β expression ( n = 3 biological replicates per group, each with 3 technical replicates). Data were expressed as mean ± SD. Statistical analysis was performed using one-way ANOVA followed by Tukey’s post hoc test. ∗∗ p < 0.01 and ∗∗∗ p < 0.001 versus the Sham-operated group; # p < 0.05 versus the tMCAO group. (E) Immunofluorescence staining for NLRP3 of brain sections in the indicated groups. Scale bars, 100 μm (main image) and 30 μm (magnified view). (F) Quantitative analysis of NLRP3 positive cells ( n = 3 biological replicates per group, each with 3 technical replicates). Data were expressed as mean ± SD. Statistical analysis was performed using one-way ANOVA followed by Tukey’s post hoc test. ∗∗∗ p < 0.001 versus the Sham-operated group; # p < 0.05 versus the tMCAO group. (G) Immunofluorescence staining for IBA-1 of brain sections in the indicated groups. Scale bars, 50 μm (main image) and 10 μm (magnified view). (H) Representative images of microglia and heat maps of Sholl analysis were shown. Scale bar, 10 μm. (I) Sholl profile shows the number of intersections at different distances from the microglial soma in the indicated groups ( n = 4 biological replicates per group, each with 3 technical replicates). Data were expressed as mean ± SD. Statistical analysis was performed using two-way ANOVA followed by Tukey’s post hoc test. ∗∗∗∗ p < 0.0001 versus the Sham-operated group; #### p < 0.0001 versus the tMCAO group. (J and K) Quantitative analysis of process length (J) and endpoints (K) per cell ( n = 4 biological replicates per group, each with 3 technical replicates). Data were expressed as mean ± SD. Statistical analysis was performed using one-way ANOVA followed by Tukey’s post hoc test. ∗∗∗ p < 0.001 versus the Sham-operated group; # p < 0.05and ## p < 0.01 versus the tMCAO group.
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    Propranolol suppressed <t>NLRP3</t> inflammasome activation in tMCAO mice (A) Western blot analysis of IBA-1, NLRP3, and IL-1β in the ischemic penumbra of different groups. (B–D) Quantitative analysis of IBA-1, NLRP3, and IL-1β expression ( n = 3 biological replicates per group, each with 3 technical replicates). Data were expressed as mean ± SD. Statistical analysis was performed using one-way ANOVA followed by Tukey’s post hoc test. ∗∗ p < 0.01 and ∗∗∗ p < 0.001 versus the Sham-operated group; # p < 0.05 versus the tMCAO group. (E) Immunofluorescence staining for NLRP3 of brain sections in the indicated groups. Scale bars, 100 μm (main image) and 30 μm (magnified view). (F) Quantitative analysis of NLRP3 positive cells ( n = 3 biological replicates per group, each with 3 technical replicates). Data were expressed as mean ± SD. Statistical analysis was performed using one-way ANOVA followed by Tukey’s post hoc test. ∗∗∗ p < 0.001 versus the Sham-operated group; # p < 0.05 versus the tMCAO group. (G) Immunofluorescence staining for IBA-1 of brain sections in the indicated groups. Scale bars, 50 μm (main image) and 10 μm (magnified view). (H) Representative images of microglia and heat maps of Sholl analysis were shown. Scale bar, 10 μm. (I) Sholl profile shows the number of intersections at different distances from the microglial soma in the indicated groups ( n = 4 biological replicates per group, each with 3 technical replicates). Data were expressed as mean ± SD. Statistical analysis was performed using two-way ANOVA followed by Tukey’s post hoc test. ∗∗∗∗ p < 0.0001 versus the Sham-operated group; #### p < 0.0001 versus the tMCAO group. (J and K) Quantitative analysis of process length (J) and endpoints (K) per cell ( n = 4 biological replicates per group, each with 3 technical replicates). Data were expressed as mean ± SD. Statistical analysis was performed using one-way ANOVA followed by Tukey’s post hoc test. ∗∗∗ p < 0.001 versus the Sham-operated group; # p < 0.05and ## p < 0.01 versus the tMCAO group.
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    Image Search Results


    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.

    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 antibodies used in this study, along with their corresponding dilution concentrations, were as follows: GAPDH (Cat No. 60004-1-Ig, ProteinTech, dilution: 1:8000), chemerin (ab72965, Abcam, dilution of 1:500), β-actin (Cat No. 81115-1-RR, ProteinTech, dilution of 1:4000), GSDMD (Cat No. 20770-1-AP, ProteinTech, dilution: 1:5000), GSDMD-N (A18281, abclonal, dilution: 1:1000), NLRP3 (bs-41293R, Bioss, dilution: 1:2000), IL-1β ( EPR21086 , Abcam, dilution: 1:1000),Caspase-1(ET1608-69, ZEN-BIOSCIENCE, 1:5000), Ecadherin (ab314063, Abcam, dilution of 1:500), N-cadherin (EPR1791-4, Abcam, dilution of 1:500), vimentin (EPR3776, Abcam, dilution of 1:500), cyclin D1 (A2708, abclonal, dilution: 1:1000), cyclin E1 (A14225, abclonal, dilution: 1:500), fatty acid synthase (FASN, 200194, ZEN-BIOSCIENCE, dilution of 1:500), and sterol regulatory element-binding protein (SREBP, Cat No. 14088-1-AP, ProteinTech, dilution of 1:4000).

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

    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.

    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 antibodies used in this study, along with their corresponding dilution concentrations, were as follows: GAPDH (Cat No. 60004-1-Ig, ProteinTech, dilution: 1:8000), chemerin (ab72965, Abcam, dilution of 1:500), β-actin (Cat No. 81115-1-RR, ProteinTech, dilution of 1:4000), GSDMD (Cat No. 20770-1-AP, ProteinTech, dilution: 1:5000), GSDMD-N (A18281, abclonal, dilution: 1:1000), NLRP3 (bs-41293R, Bioss, dilution: 1:2000), IL-1β ( EPR21086 , Abcam, dilution: 1:1000),Caspase-1(ET1608-69, ZEN-BIOSCIENCE, 1:5000), Ecadherin (ab314063, Abcam, dilution of 1:500), N-cadherin (EPR1791-4, Abcam, dilution of 1:500), vimentin (EPR3776, Abcam, dilution of 1:500), cyclin D1 (A2708, abclonal, dilution: 1:1000), cyclin E1 (A14225, abclonal, dilution: 1:500), fatty acid synthase (FASN, 200194, ZEN-BIOSCIENCE, dilution of 1:500), and sterol regulatory element-binding protein (SREBP, Cat No. 14088-1-AP, ProteinTech, dilution of 1:4000).

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

    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.

    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

    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.

    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

    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.

    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

    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.

    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

    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.

    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

    Composite hydrogel promotes the polarization of BV2 cells to M2 types and alleviates PC12 cell pyroptosis in vitro inflammatory environment. (A) Representative western blots showing protein expression of iNOS and Arg-1 in each group, β-actin was utilized as a loading control. (B) Quantitative analysis of relative expression of iNOS and Arg-1. (C) Representative immunofluorescence images of CD68 positive and iNOS positive BV2 cells (scale bar: 20 μm). (D) Representative immunofluorescence images of CD68 positive and Arg-1 positive BV2 cells (scale bar: 20 μm). (E, F) Quantitative analysis of relative fluorescence intensity of iNOS and Arg-1. (G) Representative western blots showing the expression of NLRP3, Caspase-1, IL-1β, ASC, GSDMD-N, and IL-18 protein associated with pyroptosis, β-actin was utilized as a loading control. (H) PI staining of PC12 cells in each group (scale bar, 100 μm). (I) Quantitative analysis of PI staining of PC12 cells (n = 3). (J) Quantitative analysis of relative expression of NLRP3, Caspase-1, IL-1β, ASC, GSDMD-N and IL-18 (n = 3). The data are presented as the means ± SEMs (n = 3); ∗p < 0.05, indicates significant differences; ns, is not significant. Statistical analysis was performed using two-way ANOVA followed by Tukey's multiple comparison test.

    Journal: Bioactive Materials

    Article Title: 3D-MSCs apoptotic bodies-integrated conductive hydrogel mitigates spinal cord injury via immunoregulation and alleviating neuronal pyroptosis

    doi: 10.1016/j.bioactmat.2026.01.043

    Figure Lengend Snippet: Composite hydrogel promotes the polarization of BV2 cells to M2 types and alleviates PC12 cell pyroptosis in vitro inflammatory environment. (A) Representative western blots showing protein expression of iNOS and Arg-1 in each group, β-actin was utilized as a loading control. (B) Quantitative analysis of relative expression of iNOS and Arg-1. (C) Representative immunofluorescence images of CD68 positive and iNOS positive BV2 cells (scale bar: 20 μm). (D) Representative immunofluorescence images of CD68 positive and Arg-1 positive BV2 cells (scale bar: 20 μm). (E, F) Quantitative analysis of relative fluorescence intensity of iNOS and Arg-1. (G) Representative western blots showing the expression of NLRP3, Caspase-1, IL-1β, ASC, GSDMD-N, and IL-18 protein associated with pyroptosis, β-actin was utilized as a loading control. (H) PI staining of PC12 cells in each group (scale bar, 100 μm). (I) Quantitative analysis of PI staining of PC12 cells (n = 3). (J) Quantitative analysis of relative expression of NLRP3, Caspase-1, IL-1β, ASC, GSDMD-N and IL-18 (n = 3). The data are presented as the means ± SEMs (n = 3); ∗p < 0.05, indicates significant differences; ns, is not significant. Statistical analysis was performed using two-way ANOVA followed by Tukey's multiple comparison test.

    Article Snippet: Primary antibodies against NLRP3 (cat. no. 15101) were obtained from Cell Signaling Technology (Beverly, Massachusetts, USA).

    Techniques: In Vitro, Western Blot, Expressing, Control, Immunofluorescence, Fluorescence, Staining, Comparison

    The composite hydrogel inhibits post-SCI pyroptosis in neurons. (A) Immunofluorescence images of residual neurons existing in the anterior horn of the spinal cord (scale bar, 500 μm and 200 μm). (B) Immunofluorescence image of Caspase-1 expression of neurons 3 days after SCI (scale bar, 20 μm). (C) Quantitative analysis of relative fluorescence intensity of Caspase-1 protein expression in neurons within the specified groups (n = 3). (D) Immunofluorescence image of GSDMD-N expression of neurons 3 days after SCI (scale bar, 20 μm). (E) Quantitative analysis of relative fluorescence intensity of GSDMD-N protein expression in neurons within the specified groups (n = 3). (F) Representative western blots showing the expression of NLRP3, Caspase-1, IL-1β, ASC, GSDMD-N, and IL-18 protein 3 days after SCI, GAPDH was utilized as a loading control. (G) Quantitative analysis of relative expression of NLRP3, Caspase-1, IL-1β, ASC, GSDMD-N and IL-18 (n = 3). The data are presented as the means ± SEMs (n = 3); ∗p < 0.05, indicates significant differences; ns, is not significant. Statistical analysis was performed using two-way ANOVA followed by Tukey's multiple comparison test.

    Journal: Bioactive Materials

    Article Title: 3D-MSCs apoptotic bodies-integrated conductive hydrogel mitigates spinal cord injury via immunoregulation and alleviating neuronal pyroptosis

    doi: 10.1016/j.bioactmat.2026.01.043

    Figure Lengend Snippet: The composite hydrogel inhibits post-SCI pyroptosis in neurons. (A) Immunofluorescence images of residual neurons existing in the anterior horn of the spinal cord (scale bar, 500 μm and 200 μm). (B) Immunofluorescence image of Caspase-1 expression of neurons 3 days after SCI (scale bar, 20 μm). (C) Quantitative analysis of relative fluorescence intensity of Caspase-1 protein expression in neurons within the specified groups (n = 3). (D) Immunofluorescence image of GSDMD-N expression of neurons 3 days after SCI (scale bar, 20 μm). (E) Quantitative analysis of relative fluorescence intensity of GSDMD-N protein expression in neurons within the specified groups (n = 3). (F) Representative western blots showing the expression of NLRP3, Caspase-1, IL-1β, ASC, GSDMD-N, and IL-18 protein 3 days after SCI, GAPDH was utilized as a loading control. (G) Quantitative analysis of relative expression of NLRP3, Caspase-1, IL-1β, ASC, GSDMD-N and IL-18 (n = 3). The data are presented as the means ± SEMs (n = 3); ∗p < 0.05, indicates significant differences; ns, is not significant. Statistical analysis was performed using two-way ANOVA followed by Tukey's multiple comparison test.

    Article Snippet: Primary antibodies against NLRP3 (cat. no. 15101) were obtained from Cell Signaling Technology (Beverly, Massachusetts, USA).

    Techniques: Immunofluorescence, Expressing, Fluorescence, Western Blot, Control, Comparison

    Propranolol suppressed NLRP3 inflammasome activation in tMCAO mice (A) Western blot analysis of IBA-1, NLRP3, and IL-1β in the ischemic penumbra of different groups. (B–D) Quantitative analysis of IBA-1, NLRP3, and IL-1β expression ( n = 3 biological replicates per group, each with 3 technical replicates). Data were expressed as mean ± SD. Statistical analysis was performed using one-way ANOVA followed by Tukey’s post hoc test. ∗∗ p < 0.01 and ∗∗∗ p < 0.001 versus the Sham-operated group; # p < 0.05 versus the tMCAO group. (E) Immunofluorescence staining for NLRP3 of brain sections in the indicated groups. Scale bars, 100 μm (main image) and 30 μm (magnified view). (F) Quantitative analysis of NLRP3 positive cells ( n = 3 biological replicates per group, each with 3 technical replicates). Data were expressed as mean ± SD. Statistical analysis was performed using one-way ANOVA followed by Tukey’s post hoc test. ∗∗∗ p < 0.001 versus the Sham-operated group; # p < 0.05 versus the tMCAO group. (G) Immunofluorescence staining for IBA-1 of brain sections in the indicated groups. Scale bars, 50 μm (main image) and 10 μm (magnified view). (H) Representative images of microglia and heat maps of Sholl analysis were shown. Scale bar, 10 μm. (I) Sholl profile shows the number of intersections at different distances from the microglial soma in the indicated groups ( n = 4 biological replicates per group, each with 3 technical replicates). Data were expressed as mean ± SD. Statistical analysis was performed using two-way ANOVA followed by Tukey’s post hoc test. ∗∗∗∗ p < 0.0001 versus the Sham-operated group; #### p < 0.0001 versus the tMCAO group. (J and K) Quantitative analysis of process length (J) and endpoints (K) per cell ( n = 4 biological replicates per group, each with 3 technical replicates). Data were expressed as mean ± SD. Statistical analysis was performed using one-way ANOVA followed by Tukey’s post hoc test. ∗∗∗ p < 0.001 versus the Sham-operated group; # p < 0.05and ## p < 0.01 versus the tMCAO group.

    Journal: iScience

    Article Title: Propranolol alleviates cerebral infarction through the β2-AR-mediated ERK/NLRP3 pathway

    doi: 10.1016/j.isci.2026.115779

    Figure Lengend Snippet: Propranolol suppressed NLRP3 inflammasome activation in tMCAO mice (A) Western blot analysis of IBA-1, NLRP3, and IL-1β in the ischemic penumbra of different groups. (B–D) Quantitative analysis of IBA-1, NLRP3, and IL-1β expression ( n = 3 biological replicates per group, each with 3 technical replicates). Data were expressed as mean ± SD. Statistical analysis was performed using one-way ANOVA followed by Tukey’s post hoc test. ∗∗ p < 0.01 and ∗∗∗ p < 0.001 versus the Sham-operated group; # p < 0.05 versus the tMCAO group. (E) Immunofluorescence staining for NLRP3 of brain sections in the indicated groups. Scale bars, 100 μm (main image) and 30 μm (magnified view). (F) Quantitative analysis of NLRP3 positive cells ( n = 3 biological replicates per group, each with 3 technical replicates). Data were expressed as mean ± SD. Statistical analysis was performed using one-way ANOVA followed by Tukey’s post hoc test. ∗∗∗ p < 0.001 versus the Sham-operated group; # p < 0.05 versus the tMCAO group. (G) Immunofluorescence staining for IBA-1 of brain sections in the indicated groups. Scale bars, 50 μm (main image) and 10 μm (magnified view). (H) Representative images of microglia and heat maps of Sholl analysis were shown. Scale bar, 10 μm. (I) Sholl profile shows the number of intersections at different distances from the microglial soma in the indicated groups ( n = 4 biological replicates per group, each with 3 technical replicates). Data were expressed as mean ± SD. Statistical analysis was performed using two-way ANOVA followed by Tukey’s post hoc test. ∗∗∗∗ p < 0.0001 versus the Sham-operated group; #### p < 0.0001 versus the tMCAO group. (J and K) Quantitative analysis of process length (J) and endpoints (K) per cell ( n = 4 biological replicates per group, each with 3 technical replicates). Data were expressed as mean ± SD. Statistical analysis was performed using one-way ANOVA followed by Tukey’s post hoc test. ∗∗∗ p < 0.001 versus the Sham-operated group; # p < 0.05and ## p < 0.01 versus the tMCAO group.

    Article Snippet: NLRP3 KO mice (male, 8-12 weeks old) , Jackson Laboratory , Strain #021302.

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

    NLRP3 -/- mice exhibited reduced cerebral infarction volume and attenuated BBB damage (A) TTC staining was performed to measure the cerebral infarct volume in mice. Scale bar, 5 mm. (B) Statistical analysis of infarction volume in different groups ( n = 6 mice/group). Data were expressed as mean ± SD. Statistical analysis was performed using one-way ANOVA followed by Tukey’s post hoc test. ## p < 0.01 versus the WT tMCAO group; ns, not significant. (C) Neurological function evaluation was conducted using the mNSS score ( n = 8 mice/group). Data were expressed as mean ± SD. Statistical analysis was performed using one-way ANOVA followed by Tukey’s post hoc test. # p < 0.05 versus the WT tMCAO group; ns, not significant. (D) Western blot analysis of NLRP3, IL-1β, Occludin, and ZO-1 in the ischemic penumbra of different groups. (E) Quantitative analysis of NLRP3, IL-1β, Occludin, and ZO-1 expression ( n = 3 biological replicates per group, each with 3 technical replicates). Data were expressed as mean ± SD. Statistical analysis was performed using one-way ANOVA followed by Tukey’s post hoc test. ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001 versus the WT Sham-operated group; # p < 0.05, ## p < 0.01, and #### p < 0.0001 versus the WT tMCAO group; ns, not significant. (F) Representative images of brain slices show the extravasation of EB. Scale bar, 5 mm. (G) Quantitative analysis of EB leakage in mice from different groups ( n = 4 mice/group). Data were expressed as mean ± SD. Statistical analysis was performed using one-way ANOVA followed by Tukey’s post hoc test. # p < 0.05 versus the WT tMCAO group; ns, not significant.

    Journal: iScience

    Article Title: Propranolol alleviates cerebral infarction through the β2-AR-mediated ERK/NLRP3 pathway

    doi: 10.1016/j.isci.2026.115779

    Figure Lengend Snippet: NLRP3 -/- mice exhibited reduced cerebral infarction volume and attenuated BBB damage (A) TTC staining was performed to measure the cerebral infarct volume in mice. Scale bar, 5 mm. (B) Statistical analysis of infarction volume in different groups ( n = 6 mice/group). Data were expressed as mean ± SD. Statistical analysis was performed using one-way ANOVA followed by Tukey’s post hoc test. ## p < 0.01 versus the WT tMCAO group; ns, not significant. (C) Neurological function evaluation was conducted using the mNSS score ( n = 8 mice/group). Data were expressed as mean ± SD. Statistical analysis was performed using one-way ANOVA followed by Tukey’s post hoc test. # p < 0.05 versus the WT tMCAO group; ns, not significant. (D) Western blot analysis of NLRP3, IL-1β, Occludin, and ZO-1 in the ischemic penumbra of different groups. (E) Quantitative analysis of NLRP3, IL-1β, Occludin, and ZO-1 expression ( n = 3 biological replicates per group, each with 3 technical replicates). Data were expressed as mean ± SD. Statistical analysis was performed using one-way ANOVA followed by Tukey’s post hoc test. ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001 versus the WT Sham-operated group; # p < 0.05, ## p < 0.01, and #### p < 0.0001 versus the WT tMCAO group; ns, not significant. (F) Representative images of brain slices show the extravasation of EB. Scale bar, 5 mm. (G) Quantitative analysis of EB leakage in mice from different groups ( n = 4 mice/group). Data were expressed as mean ± SD. Statistical analysis was performed using one-way ANOVA followed by Tukey’s post hoc test. # p < 0.05 versus the WT tMCAO group; ns, not significant.

    Article Snippet: NLRP3 KO mice (male, 8-12 weeks old) , Jackson Laboratory , Strain #021302.

    Techniques: Staining, Western Blot, Expressing

    Knockout of NLRP3 alleviated BBB damage and the activation of microglia caused by tMCAO (A) Immunofluorescence staining for IBA-1 of brain sections in the indicated groups. Scale bars, 50 μm (main image) and 10 μm (magnified view). (B) Representative images of microglia and heat maps of Sholl analysis were shown. Scale bar, 10 μm. (C) Sholl profile shows the number of intersections at different distances from the microglial soma in the indicated groups ( n = 4 biological replicates per group, each with 3 technical replicates). Data were expressed as mean ± SD. Statistical analysis was performed using two-way ANOVA followed by Tukey’s post hoc test. ∗∗∗∗ p < 0.0001 versus the WT Sham-operated group; #### p < 0.0001 versus the WT tMCAO group. (D and E) Quantitative analysis of process length (D) and endpoints (E) per cell ( n = 4 biological replicates per group, each with 3 technical replicates). Data were expressed as mean ± SD. Statistical analysis was performed using one-way ANOVA followed by Tukey’s post hoc test. ∗∗∗ p < 0.001 versus the WT Sham-operated group; # p < 0.05 versus the WT tMCAO group; ns, not significant. (F) Immunofluorescence staining for CD-31 of brain sections of the indicated groups. Scale bars, 100 μm (main image) and 30 μm (magnified view). (G) Statistical analysis of CD-31 positive cells ( n = 3 biological replicates per group, each with 3 technical replicates). Data were expressed as mean ± SD. Statistical analysis was performed using one-way ANOVA followed by Tukey’s post hoc test. ∗∗∗ p < 0.001 versus the WT Sham-operated group; # p < 0.05 versus the WT tMCAO group; ns, not significant.

    Journal: iScience

    Article Title: Propranolol alleviates cerebral infarction through the β2-AR-mediated ERK/NLRP3 pathway

    doi: 10.1016/j.isci.2026.115779

    Figure Lengend Snippet: Knockout of NLRP3 alleviated BBB damage and the activation of microglia caused by tMCAO (A) Immunofluorescence staining for IBA-1 of brain sections in the indicated groups. Scale bars, 50 μm (main image) and 10 μm (magnified view). (B) Representative images of microglia and heat maps of Sholl analysis were shown. Scale bar, 10 μm. (C) Sholl profile shows the number of intersections at different distances from the microglial soma in the indicated groups ( n = 4 biological replicates per group, each with 3 technical replicates). Data were expressed as mean ± SD. Statistical analysis was performed using two-way ANOVA followed by Tukey’s post hoc test. ∗∗∗∗ p < 0.0001 versus the WT Sham-operated group; #### p < 0.0001 versus the WT tMCAO group. (D and E) Quantitative analysis of process length (D) and endpoints (E) per cell ( n = 4 biological replicates per group, each with 3 technical replicates). Data were expressed as mean ± SD. Statistical analysis was performed using one-way ANOVA followed by Tukey’s post hoc test. ∗∗∗ p < 0.001 versus the WT Sham-operated group; # p < 0.05 versus the WT tMCAO group; ns, not significant. (F) Immunofluorescence staining for CD-31 of brain sections of the indicated groups. Scale bars, 100 μm (main image) and 30 μm (magnified view). (G) Statistical analysis of CD-31 positive cells ( n = 3 biological replicates per group, each with 3 technical replicates). Data were expressed as mean ± SD. Statistical analysis was performed using one-way ANOVA followed by Tukey’s post hoc test. ∗∗∗ p < 0.001 versus the WT Sham-operated group; # p < 0.05 versus the WT tMCAO group; ns, not significant.

    Article Snippet: NLRP3 KO mice (male, 8-12 weeks old) , Jackson Laboratory , Strain #021302.

    Techniques: Knock-Out, Activation Assay, Immunofluorescence, Staining

    Propranolol reduced the expression of NLRP3 and IL-1β in BV2 cells subjected to OGD/R (A) Schematic of cell experiment steps. (B) Western blot analysis of NLRP3 and IL-1β in BV2 cells at 4, 6, 8, 12, and 24 h after OGD/R. (C and D) Quantitative analysis of NLRP3 and IL-1β expression ( n = 3 biological replicates per group, each with 3 technical replicates). Data were expressed as mean ± SD. Statistical analysis was performed using one-way ANOVA followed by Tukey’s post hoc test. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001 versus the control group. (E) Western blot analysis of NLRP3 and IL-1β in BV2 cells of different treatment groups. (F and G) Quantitative analysis of NLRP3 and IL-1β expression ( n = 3 biological replicates per group, each with 3 technical replicates). Data were expressed as mean ± SD. Statistical analysis was performed using one-way ANOVA followed by Tukey’s post hoc test. ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001 versus the control group; # p < 0.05 and ## p < 0.01 versus the OGD/R group.

    Journal: iScience

    Article Title: Propranolol alleviates cerebral infarction through the β2-AR-mediated ERK/NLRP3 pathway

    doi: 10.1016/j.isci.2026.115779

    Figure Lengend Snippet: Propranolol reduced the expression of NLRP3 and IL-1β in BV2 cells subjected to OGD/R (A) Schematic of cell experiment steps. (B) Western blot analysis of NLRP3 and IL-1β in BV2 cells at 4, 6, 8, 12, and 24 h after OGD/R. (C and D) Quantitative analysis of NLRP3 and IL-1β expression ( n = 3 biological replicates per group, each with 3 technical replicates). Data were expressed as mean ± SD. Statistical analysis was performed using one-way ANOVA followed by Tukey’s post hoc test. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001 versus the control group. (E) Western blot analysis of NLRP3 and IL-1β in BV2 cells of different treatment groups. (F and G) Quantitative analysis of NLRP3 and IL-1β expression ( n = 3 biological replicates per group, each with 3 technical replicates). Data were expressed as mean ± SD. Statistical analysis was performed using one-way ANOVA followed by Tukey’s post hoc test. ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001 versus the control group; # p < 0.05 and ## p < 0.01 versus the OGD/R group.

    Article Snippet: NLRP3 KO mice (male, 8-12 weeks old) , Jackson Laboratory , Strain #021302.

    Techniques: Expressing, Western Blot, Control

    Blockade of β2-AR reduced the expression of NLRP3 in BV2 cells subjected to OGD/R (A) Western blot analysis of the effects of dobutamine and betaxolol on NLRP3 and IL-1β expression in BV2 cells. (B and C) Quantitative analysis of NLRP3 and IL-1β expression ( n = 3 biological replicates per group, each with 3 technical replicates). Data were expressed as mean ± SD. Statistical analysis was performed using one-way ANOVA followed by Tukey’s post hoc test. ∗∗∗ p < 0.001 versus the control group. (D) Western blot analysis of salmeterol and ICI118,551 on NLRP3 and IL-1β expression in BV2 cells. (E and F) Quantitative analysis of NLRP3 and IL-1β expression ( n = 3 biological replicates per group, each with 3 technical replicates). Data were expressed as mean ± SD. Statistical analysis was performed using one-way ANOVA followed by Tukey’s post hoc test. ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001 versus the control group; # p < 0.05 and ## p < 0.01 versus the OGD/R group.

    Journal: iScience

    Article Title: Propranolol alleviates cerebral infarction through the β2-AR-mediated ERK/NLRP3 pathway

    doi: 10.1016/j.isci.2026.115779

    Figure Lengend Snippet: Blockade of β2-AR reduced the expression of NLRP3 in BV2 cells subjected to OGD/R (A) Western blot analysis of the effects of dobutamine and betaxolol on NLRP3 and IL-1β expression in BV2 cells. (B and C) Quantitative analysis of NLRP3 and IL-1β expression ( n = 3 biological replicates per group, each with 3 technical replicates). Data were expressed as mean ± SD. Statistical analysis was performed using one-way ANOVA followed by Tukey’s post hoc test. ∗∗∗ p < 0.001 versus the control group. (D) Western blot analysis of salmeterol and ICI118,551 on NLRP3 and IL-1β expression in BV2 cells. (E and F) Quantitative analysis of NLRP3 and IL-1β expression ( n = 3 biological replicates per group, each with 3 technical replicates). Data were expressed as mean ± SD. Statistical analysis was performed using one-way ANOVA followed by Tukey’s post hoc test. ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001 versus the control group; # p < 0.05 and ## p < 0.01 versus the OGD/R group.

    Article Snippet: NLRP3 KO mice (male, 8-12 weeks old) , Jackson Laboratory , Strain #021302.

    Techniques: Expressing, Western Blot, Control

    Activation of β2-AR induced the expression of NLRP3 and IL-1β via the ERK1/2 MAPK signaling pathway (A) Western blot analysis of the effects of H-89 and U0126 on NLRP3 and IL-1β expression in BV2 cells. (B and C) Quantitative analysis of NLRP3 and IL-1β expression ( n = 3 biological replicates per group, each with 3 technical replicates). Data were expressed as mean ± SD. Statistical analysis was performed using one-way ANOVA followed by Tukey’s post hoc test. ∗∗ p < 0.01 and ∗∗∗ p < 0.001 versus the control group; # p < 0.05 versus the OGD/R group. (D) Western blot analysis of p -ERK1/2 expression in BV2 cells. (E) Quantitative analysis of p -ERK1/2 expression ( n = 3 biological replicates per group, each with 3 technical replicates). Data were expressed as mean ± SD. Statistical analysis was performed using one-way ANOVA followed by Tukey’s post hoc test. ∗∗ p < 0.01 and ∗∗∗ p < 0.001 versus the control group; # p < 0.05 versus the OGD/R group.

    Journal: iScience

    Article Title: Propranolol alleviates cerebral infarction through the β2-AR-mediated ERK/NLRP3 pathway

    doi: 10.1016/j.isci.2026.115779

    Figure Lengend Snippet: Activation of β2-AR induced the expression of NLRP3 and IL-1β via the ERK1/2 MAPK signaling pathway (A) Western blot analysis of the effects of H-89 and U0126 on NLRP3 and IL-1β expression in BV2 cells. (B and C) Quantitative analysis of NLRP3 and IL-1β expression ( n = 3 biological replicates per group, each with 3 technical replicates). Data were expressed as mean ± SD. Statistical analysis was performed using one-way ANOVA followed by Tukey’s post hoc test. ∗∗ p < 0.01 and ∗∗∗ p < 0.001 versus the control group; # p < 0.05 versus the OGD/R group. (D) Western blot analysis of p -ERK1/2 expression in BV2 cells. (E) Quantitative analysis of p -ERK1/2 expression ( n = 3 biological replicates per group, each with 3 technical replicates). Data were expressed as mean ± SD. Statistical analysis was performed using one-way ANOVA followed by Tukey’s post hoc test. ∗∗ p < 0.01 and ∗∗∗ p < 0.001 versus the control group; # p < 0.05 versus the OGD/R group.

    Article Snippet: NLRP3 KO mice (male, 8-12 weeks old) , Jackson Laboratory , Strain #021302.

    Techniques: Activation Assay, Expressing, Western Blot, Control

    Propranolol suppressed NLRP3 inflammasome activation in tMCAO mice (A) Western blot analysis of IBA-1, NLRP3, and IL-1β in the ischemic penumbra of different groups. (B–D) Quantitative analysis of IBA-1, NLRP3, and IL-1β expression ( n = 3 biological replicates per group, each with 3 technical replicates). Data were expressed as mean ± SD. Statistical analysis was performed using one-way ANOVA followed by Tukey’s post hoc test. ∗∗ p < 0.01 and ∗∗∗ p < 0.001 versus the Sham-operated group; # p < 0.05 versus the tMCAO group. (E) Immunofluorescence staining for NLRP3 of brain sections in the indicated groups. Scale bars, 100 μm (main image) and 30 μm (magnified view). (F) Quantitative analysis of NLRP3 positive cells ( n = 3 biological replicates per group, each with 3 technical replicates). Data were expressed as mean ± SD. Statistical analysis was performed using one-way ANOVA followed by Tukey’s post hoc test. ∗∗∗ p < 0.001 versus the Sham-operated group; # p < 0.05 versus the tMCAO group. (G) Immunofluorescence staining for IBA-1 of brain sections in the indicated groups. Scale bars, 50 μm (main image) and 10 μm (magnified view). (H) Representative images of microglia and heat maps of Sholl analysis were shown. Scale bar, 10 μm. (I) Sholl profile shows the number of intersections at different distances from the microglial soma in the indicated groups ( n = 4 biological replicates per group, each with 3 technical replicates). Data were expressed as mean ± SD. Statistical analysis was performed using two-way ANOVA followed by Tukey’s post hoc test. ∗∗∗∗ p < 0.0001 versus the Sham-operated group; #### p < 0.0001 versus the tMCAO group. (J and K) Quantitative analysis of process length (J) and endpoints (K) per cell ( n = 4 biological replicates per group, each with 3 technical replicates). Data were expressed as mean ± SD. Statistical analysis was performed using one-way ANOVA followed by Tukey’s post hoc test. ∗∗∗ p < 0.001 versus the Sham-operated group; # p < 0.05and ## p < 0.01 versus the tMCAO group.

    Journal: iScience

    Article Title: Propranolol alleviates cerebral infarction through the β2-AR-mediated ERK/NLRP3 pathway

    doi: 10.1016/j.isci.2026.115779

    Figure Lengend Snippet: Propranolol suppressed NLRP3 inflammasome activation in tMCAO mice (A) Western blot analysis of IBA-1, NLRP3, and IL-1β in the ischemic penumbra of different groups. (B–D) Quantitative analysis of IBA-1, NLRP3, and IL-1β expression ( n = 3 biological replicates per group, each with 3 technical replicates). Data were expressed as mean ± SD. Statistical analysis was performed using one-way ANOVA followed by Tukey’s post hoc test. ∗∗ p < 0.01 and ∗∗∗ p < 0.001 versus the Sham-operated group; # p < 0.05 versus the tMCAO group. (E) Immunofluorescence staining for NLRP3 of brain sections in the indicated groups. Scale bars, 100 μm (main image) and 30 μm (magnified view). (F) Quantitative analysis of NLRP3 positive cells ( n = 3 biological replicates per group, each with 3 technical replicates). Data were expressed as mean ± SD. Statistical analysis was performed using one-way ANOVA followed by Tukey’s post hoc test. ∗∗∗ p < 0.001 versus the Sham-operated group; # p < 0.05 versus the tMCAO group. (G) Immunofluorescence staining for IBA-1 of brain sections in the indicated groups. Scale bars, 50 μm (main image) and 10 μm (magnified view). (H) Representative images of microglia and heat maps of Sholl analysis were shown. Scale bar, 10 μm. (I) Sholl profile shows the number of intersections at different distances from the microglial soma in the indicated groups ( n = 4 biological replicates per group, each with 3 technical replicates). Data were expressed as mean ± SD. Statistical analysis was performed using two-way ANOVA followed by Tukey’s post hoc test. ∗∗∗∗ p < 0.0001 versus the Sham-operated group; #### p < 0.0001 versus the tMCAO group. (J and K) Quantitative analysis of process length (J) and endpoints (K) per cell ( n = 4 biological replicates per group, each with 3 technical replicates). Data were expressed as mean ± SD. Statistical analysis was performed using one-way ANOVA followed by Tukey’s post hoc test. ∗∗∗ p < 0.001 versus the Sham-operated group; # p < 0.05and ## p < 0.01 versus the tMCAO group.

    Article Snippet: Male C57BL/6J mice aged 8-12 weeks were purchased from the Model Animal Research Center of Nanjing University (Nanjing, China), while NLRP3 KO (NLRP3 -/- ) mice with C57BL/6 background were purchased from Jackson Laboratory.

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

    NLRP3 -/- mice exhibited reduced cerebral infarction volume and attenuated BBB damage (A) TTC staining was performed to measure the cerebral infarct volume in mice. Scale bar, 5 mm. (B) Statistical analysis of infarction volume in different groups ( n = 6 mice/group). Data were expressed as mean ± SD. Statistical analysis was performed using one-way ANOVA followed by Tukey’s post hoc test. ## p < 0.01 versus the WT tMCAO group; ns, not significant. (C) Neurological function evaluation was conducted using the mNSS score ( n = 8 mice/group). Data were expressed as mean ± SD. Statistical analysis was performed using one-way ANOVA followed by Tukey’s post hoc test. # p < 0.05 versus the WT tMCAO group; ns, not significant. (D) Western blot analysis of NLRP3, IL-1β, Occludin, and ZO-1 in the ischemic penumbra of different groups. (E) Quantitative analysis of NLRP3, IL-1β, Occludin, and ZO-1 expression ( n = 3 biological replicates per group, each with 3 technical replicates). Data were expressed as mean ± SD. Statistical analysis was performed using one-way ANOVA followed by Tukey’s post hoc test. ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001 versus the WT Sham-operated group; # p < 0.05, ## p < 0.01, and #### p < 0.0001 versus the WT tMCAO group; ns, not significant. (F) Representative images of brain slices show the extravasation of EB. Scale bar, 5 mm. (G) Quantitative analysis of EB leakage in mice from different groups ( n = 4 mice/group). Data were expressed as mean ± SD. Statistical analysis was performed using one-way ANOVA followed by Tukey’s post hoc test. # p < 0.05 versus the WT tMCAO group; ns, not significant.

    Journal: iScience

    Article Title: Propranolol alleviates cerebral infarction through the β2-AR-mediated ERK/NLRP3 pathway

    doi: 10.1016/j.isci.2026.115779

    Figure Lengend Snippet: NLRP3 -/- mice exhibited reduced cerebral infarction volume and attenuated BBB damage (A) TTC staining was performed to measure the cerebral infarct volume in mice. Scale bar, 5 mm. (B) Statistical analysis of infarction volume in different groups ( n = 6 mice/group). Data were expressed as mean ± SD. Statistical analysis was performed using one-way ANOVA followed by Tukey’s post hoc test. ## p < 0.01 versus the WT tMCAO group; ns, not significant. (C) Neurological function evaluation was conducted using the mNSS score ( n = 8 mice/group). Data were expressed as mean ± SD. Statistical analysis was performed using one-way ANOVA followed by Tukey’s post hoc test. # p < 0.05 versus the WT tMCAO group; ns, not significant. (D) Western blot analysis of NLRP3, IL-1β, Occludin, and ZO-1 in the ischemic penumbra of different groups. (E) Quantitative analysis of NLRP3, IL-1β, Occludin, and ZO-1 expression ( n = 3 biological replicates per group, each with 3 technical replicates). Data were expressed as mean ± SD. Statistical analysis was performed using one-way ANOVA followed by Tukey’s post hoc test. ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001 versus the WT Sham-operated group; # p < 0.05, ## p < 0.01, and #### p < 0.0001 versus the WT tMCAO group; ns, not significant. (F) Representative images of brain slices show the extravasation of EB. Scale bar, 5 mm. (G) Quantitative analysis of EB leakage in mice from different groups ( n = 4 mice/group). Data were expressed as mean ± SD. Statistical analysis was performed using one-way ANOVA followed by Tukey’s post hoc test. # p < 0.05 versus the WT tMCAO group; ns, not significant.

    Article Snippet: Male C57BL/6J mice aged 8-12 weeks were purchased from the Model Animal Research Center of Nanjing University (Nanjing, China), while NLRP3 KO (NLRP3 -/- ) mice with C57BL/6 background were purchased from Jackson Laboratory.

    Techniques: Staining, Western Blot, Expressing

    Knockout of NLRP3 alleviated BBB damage and the activation of microglia caused by tMCAO (A) Immunofluorescence staining for IBA-1 of brain sections in the indicated groups. Scale bars, 50 μm (main image) and 10 μm (magnified view). (B) Representative images of microglia and heat maps of Sholl analysis were shown. Scale bar, 10 μm. (C) Sholl profile shows the number of intersections at different distances from the microglial soma in the indicated groups ( n = 4 biological replicates per group, each with 3 technical replicates). Data were expressed as mean ± SD. Statistical analysis was performed using two-way ANOVA followed by Tukey’s post hoc test. ∗∗∗∗ p < 0.0001 versus the WT Sham-operated group; #### p < 0.0001 versus the WT tMCAO group. (D and E) Quantitative analysis of process length (D) and endpoints (E) per cell ( n = 4 biological replicates per group, each with 3 technical replicates). Data were expressed as mean ± SD. Statistical analysis was performed using one-way ANOVA followed by Tukey’s post hoc test. ∗∗∗ p < 0.001 versus the WT Sham-operated group; # p < 0.05 versus the WT tMCAO group; ns, not significant. (F) Immunofluorescence staining for CD-31 of brain sections of the indicated groups. Scale bars, 100 μm (main image) and 30 μm (magnified view). (G) Statistical analysis of CD-31 positive cells ( n = 3 biological replicates per group, each with 3 technical replicates). Data were expressed as mean ± SD. Statistical analysis was performed using one-way ANOVA followed by Tukey’s post hoc test. ∗∗∗ p < 0.001 versus the WT Sham-operated group; # p < 0.05 versus the WT tMCAO group; ns, not significant.

    Journal: iScience

    Article Title: Propranolol alleviates cerebral infarction through the β2-AR-mediated ERK/NLRP3 pathway

    doi: 10.1016/j.isci.2026.115779

    Figure Lengend Snippet: Knockout of NLRP3 alleviated BBB damage and the activation of microglia caused by tMCAO (A) Immunofluorescence staining for IBA-1 of brain sections in the indicated groups. Scale bars, 50 μm (main image) and 10 μm (magnified view). (B) Representative images of microglia and heat maps of Sholl analysis were shown. Scale bar, 10 μm. (C) Sholl profile shows the number of intersections at different distances from the microglial soma in the indicated groups ( n = 4 biological replicates per group, each with 3 technical replicates). Data were expressed as mean ± SD. Statistical analysis was performed using two-way ANOVA followed by Tukey’s post hoc test. ∗∗∗∗ p < 0.0001 versus the WT Sham-operated group; #### p < 0.0001 versus the WT tMCAO group. (D and E) Quantitative analysis of process length (D) and endpoints (E) per cell ( n = 4 biological replicates per group, each with 3 technical replicates). Data were expressed as mean ± SD. Statistical analysis was performed using one-way ANOVA followed by Tukey’s post hoc test. ∗∗∗ p < 0.001 versus the WT Sham-operated group; # p < 0.05 versus the WT tMCAO group; ns, not significant. (F) Immunofluorescence staining for CD-31 of brain sections of the indicated groups. Scale bars, 100 μm (main image) and 30 μm (magnified view). (G) Statistical analysis of CD-31 positive cells ( n = 3 biological replicates per group, each with 3 technical replicates). Data were expressed as mean ± SD. Statistical analysis was performed using one-way ANOVA followed by Tukey’s post hoc test. ∗∗∗ p < 0.001 versus the WT Sham-operated group; # p < 0.05 versus the WT tMCAO group; ns, not significant.

    Article Snippet: Male C57BL/6J mice aged 8-12 weeks were purchased from the Model Animal Research Center of Nanjing University (Nanjing, China), while NLRP3 KO (NLRP3 -/- ) mice with C57BL/6 background were purchased from Jackson Laboratory.

    Techniques: Knock-Out, Activation Assay, Immunofluorescence, Staining

    Propranolol reduced the expression of NLRP3 and IL-1β in BV2 cells subjected to OGD/R (A) Schematic of cell experiment steps. (B) Western blot analysis of NLRP3 and IL-1β in BV2 cells at 4, 6, 8, 12, and 24 h after OGD/R. (C and D) Quantitative analysis of NLRP3 and IL-1β expression ( n = 3 biological replicates per group, each with 3 technical replicates). Data were expressed as mean ± SD. Statistical analysis was performed using one-way ANOVA followed by Tukey’s post hoc test. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001 versus the control group. (E) Western blot analysis of NLRP3 and IL-1β in BV2 cells of different treatment groups. (F and G) Quantitative analysis of NLRP3 and IL-1β expression ( n = 3 biological replicates per group, each with 3 technical replicates). Data were expressed as mean ± SD. Statistical analysis was performed using one-way ANOVA followed by Tukey’s post hoc test. ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001 versus the control group; # p < 0.05 and ## p < 0.01 versus the OGD/R group.

    Journal: iScience

    Article Title: Propranolol alleviates cerebral infarction through the β2-AR-mediated ERK/NLRP3 pathway

    doi: 10.1016/j.isci.2026.115779

    Figure Lengend Snippet: Propranolol reduced the expression of NLRP3 and IL-1β in BV2 cells subjected to OGD/R (A) Schematic of cell experiment steps. (B) Western blot analysis of NLRP3 and IL-1β in BV2 cells at 4, 6, 8, 12, and 24 h after OGD/R. (C and D) Quantitative analysis of NLRP3 and IL-1β expression ( n = 3 biological replicates per group, each with 3 technical replicates). Data were expressed as mean ± SD. Statistical analysis was performed using one-way ANOVA followed by Tukey’s post hoc test. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001 versus the control group. (E) Western blot analysis of NLRP3 and IL-1β in BV2 cells of different treatment groups. (F and G) Quantitative analysis of NLRP3 and IL-1β expression ( n = 3 biological replicates per group, each with 3 technical replicates). Data were expressed as mean ± SD. Statistical analysis was performed using one-way ANOVA followed by Tukey’s post hoc test. ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001 versus the control group; # p < 0.05 and ## p < 0.01 versus the OGD/R group.

    Article Snippet: Male C57BL/6J mice aged 8-12 weeks were purchased from the Model Animal Research Center of Nanjing University (Nanjing, China), while NLRP3 KO (NLRP3 -/- ) mice with C57BL/6 background were purchased from Jackson Laboratory.

    Techniques: Expressing, Western Blot, Control

    Blockade of β2-AR reduced the expression of NLRP3 in BV2 cells subjected to OGD/R (A) Western blot analysis of the effects of dobutamine and betaxolol on NLRP3 and IL-1β expression in BV2 cells. (B and C) Quantitative analysis of NLRP3 and IL-1β expression ( n = 3 biological replicates per group, each with 3 technical replicates). Data were expressed as mean ± SD. Statistical analysis was performed using one-way ANOVA followed by Tukey’s post hoc test. ∗∗∗ p < 0.001 versus the control group. (D) Western blot analysis of salmeterol and ICI118,551 on NLRP3 and IL-1β expression in BV2 cells. (E and F) Quantitative analysis of NLRP3 and IL-1β expression ( n = 3 biological replicates per group, each with 3 technical replicates). Data were expressed as mean ± SD. Statistical analysis was performed using one-way ANOVA followed by Tukey’s post hoc test. ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001 versus the control group; # p < 0.05 and ## p < 0.01 versus the OGD/R group.

    Journal: iScience

    Article Title: Propranolol alleviates cerebral infarction through the β2-AR-mediated ERK/NLRP3 pathway

    doi: 10.1016/j.isci.2026.115779

    Figure Lengend Snippet: Blockade of β2-AR reduced the expression of NLRP3 in BV2 cells subjected to OGD/R (A) Western blot analysis of the effects of dobutamine and betaxolol on NLRP3 and IL-1β expression in BV2 cells. (B and C) Quantitative analysis of NLRP3 and IL-1β expression ( n = 3 biological replicates per group, each with 3 technical replicates). Data were expressed as mean ± SD. Statistical analysis was performed using one-way ANOVA followed by Tukey’s post hoc test. ∗∗∗ p < 0.001 versus the control group. (D) Western blot analysis of salmeterol and ICI118,551 on NLRP3 and IL-1β expression in BV2 cells. (E and F) Quantitative analysis of NLRP3 and IL-1β expression ( n = 3 biological replicates per group, each with 3 technical replicates). Data were expressed as mean ± SD. Statistical analysis was performed using one-way ANOVA followed by Tukey’s post hoc test. ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001 versus the control group; # p < 0.05 and ## p < 0.01 versus the OGD/R group.

    Article Snippet: Male C57BL/6J mice aged 8-12 weeks were purchased from the Model Animal Research Center of Nanjing University (Nanjing, China), while NLRP3 KO (NLRP3 -/- ) mice with C57BL/6 background were purchased from Jackson Laboratory.

    Techniques: Expressing, Western Blot, Control

    Activation of β2-AR induced the expression of NLRP3 and IL-1β via the ERK1/2 MAPK signaling pathway (A) Western blot analysis of the effects of H-89 and U0126 on NLRP3 and IL-1β expression in BV2 cells. (B and C) Quantitative analysis of NLRP3 and IL-1β expression ( n = 3 biological replicates per group, each with 3 technical replicates). Data were expressed as mean ± SD. Statistical analysis was performed using one-way ANOVA followed by Tukey’s post hoc test. ∗∗ p < 0.01 and ∗∗∗ p < 0.001 versus the control group; # p < 0.05 versus the OGD/R group. (D) Western blot analysis of p -ERK1/2 expression in BV2 cells. (E) Quantitative analysis of p -ERK1/2 expression ( n = 3 biological replicates per group, each with 3 technical replicates). Data were expressed as mean ± SD. Statistical analysis was performed using one-way ANOVA followed by Tukey’s post hoc test. ∗∗ p < 0.01 and ∗∗∗ p < 0.001 versus the control group; # p < 0.05 versus the OGD/R group.

    Journal: iScience

    Article Title: Propranolol alleviates cerebral infarction through the β2-AR-mediated ERK/NLRP3 pathway

    doi: 10.1016/j.isci.2026.115779

    Figure Lengend Snippet: Activation of β2-AR induced the expression of NLRP3 and IL-1β via the ERK1/2 MAPK signaling pathway (A) Western blot analysis of the effects of H-89 and U0126 on NLRP3 and IL-1β expression in BV2 cells. (B and C) Quantitative analysis of NLRP3 and IL-1β expression ( n = 3 biological replicates per group, each with 3 technical replicates). Data were expressed as mean ± SD. Statistical analysis was performed using one-way ANOVA followed by Tukey’s post hoc test. ∗∗ p < 0.01 and ∗∗∗ p < 0.001 versus the control group; # p < 0.05 versus the OGD/R group. (D) Western blot analysis of p -ERK1/2 expression in BV2 cells. (E) Quantitative analysis of p -ERK1/2 expression ( n = 3 biological replicates per group, each with 3 technical replicates). Data were expressed as mean ± SD. Statistical analysis was performed using one-way ANOVA followed by Tukey’s post hoc test. ∗∗ p < 0.01 and ∗∗∗ p < 0.001 versus the control group; # p < 0.05 versus the OGD/R group.

    Article Snippet: Male C57BL/6J mice aged 8-12 weeks were purchased from the Model Animal Research Center of Nanjing University (Nanjing, China), while NLRP3 KO (NLRP3 -/- ) mice with C57BL/6 background were purchased from Jackson Laboratory.

    Techniques: Activation Assay, Expressing, Western Blot, Control