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cleaved caspase 1  (MedChemExpress)


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    Structured Review

    MedChemExpress cleaved caspase 1
    Schematic illustration of the mechanism of ZIF-8@Que nanoparticles in GC treatment. ZIF-8@Que nanoparticles were prepared via a one-pot co-precipitation process, encapsulating quercetin within the ZIF-8 framework. Upon systemic administration, ZIF-8@Que preferentially accumulates in gastric tumors and undergoes acidic pH-triggered drug release. The nanoparticles exhibit intrinsic POD-like activity, catalyzing H 2 O 2 to generate ROS, which disrupt mitochondrial function by collapsing Δψm, depleting ATP, and enhancing oxidative stress. ROS-driven mitochondrial injury subsequently activates inflammasome-dependent <t>caspase-1,</t> leading to GSDMD cleavage, pore formation, release of IL-1β and IL-18, and subsequent pyroptotic cell death. This cascade culminates in robust eradication of GC cells while sparing normal tissues, highlighting the therapeutic promise of ZIF-8@Que as pyroptosis-inducing nanoparticles.
    Cleaved Caspase 1, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 28 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/cleaved caspase 1/product/MedChemExpress
    Average 94 stars, based on 28 article reviews
    cleaved caspase 1 - by Bioz Stars, 2026-02
    94/100 stars

    Images

    1) Product Images from "pH-responsive ZIF-8@quercetin nanoparticles induce pyroptosis for targeted gastric cancer therapy"

    Article Title: pH-responsive ZIF-8@quercetin nanoparticles induce pyroptosis for targeted gastric cancer therapy

    Journal: Materials Today Bio

    doi: 10.1016/j.mtbio.2026.102806

    Schematic illustration of the mechanism of ZIF-8@Que nanoparticles in GC treatment. ZIF-8@Que nanoparticles were prepared via a one-pot co-precipitation process, encapsulating quercetin within the ZIF-8 framework. Upon systemic administration, ZIF-8@Que preferentially accumulates in gastric tumors and undergoes acidic pH-triggered drug release. The nanoparticles exhibit intrinsic POD-like activity, catalyzing H 2 O 2 to generate ROS, which disrupt mitochondrial function by collapsing Δψm, depleting ATP, and enhancing oxidative stress. ROS-driven mitochondrial injury subsequently activates inflammasome-dependent caspase-1, leading to GSDMD cleavage, pore formation, release of IL-1β and IL-18, and subsequent pyroptotic cell death. This cascade culminates in robust eradication of GC cells while sparing normal tissues, highlighting the therapeutic promise of ZIF-8@Que as pyroptosis-inducing nanoparticles.
    Figure Legend Snippet: Schematic illustration of the mechanism of ZIF-8@Que nanoparticles in GC treatment. ZIF-8@Que nanoparticles were prepared via a one-pot co-precipitation process, encapsulating quercetin within the ZIF-8 framework. Upon systemic administration, ZIF-8@Que preferentially accumulates in gastric tumors and undergoes acidic pH-triggered drug release. The nanoparticles exhibit intrinsic POD-like activity, catalyzing H 2 O 2 to generate ROS, which disrupt mitochondrial function by collapsing Δψm, depleting ATP, and enhancing oxidative stress. ROS-driven mitochondrial injury subsequently activates inflammasome-dependent caspase-1, leading to GSDMD cleavage, pore formation, release of IL-1β and IL-18, and subsequent pyroptotic cell death. This cascade culminates in robust eradication of GC cells while sparing normal tissues, highlighting the therapeutic promise of ZIF-8@Que as pyroptosis-inducing nanoparticles.

    Techniques Used: Activity Assay

    In vivo therapeutic efficacy and safety profile of ZIF-8@Que. (A) Hemolysis assay of mouse RBCs incubated with ZIF-8@Que at various concentrations. (B, C) Assessment of systemic toxicity in healthy mice: body weight (B) and serum biochemical (C) of C57BL/6 mice receiving repeated intravenous doses of ZIF-8@Que (50 mg/kg, once weekly for 4 weeks). (D) H&E staining of major organs confirming normal histology. Scale bar = 10 μm. (E) Experimental timeline for tumor establishment and treatment in nude mice. (F) Body weight of tumor-bearing mice during therapy. (G, H) Tumor growth curves (G) and tumor weight curves (H) for each group at different time points. (I) Kaplan-Meier survival curves for each group. (J) Representative tumor images at study endpoint. (K) H&E staining showing extensive necrosis in ZIF-8@Que-treated tumors. (L) Representative images of Ki67, cleaved caspase-1, cleaved caspase-3, cleaved GSDMD and TUNEL in tumor tissues, highlighting pyroptosis-mediated antitumor effects. For all studies, n ≥ 3. Data are shown as the mean ± SD. Comparisons were performed using the student's t-test or ANOVA. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, or ns = not significant.
    Figure Legend Snippet: In vivo therapeutic efficacy and safety profile of ZIF-8@Que. (A) Hemolysis assay of mouse RBCs incubated with ZIF-8@Que at various concentrations. (B, C) Assessment of systemic toxicity in healthy mice: body weight (B) and serum biochemical (C) of C57BL/6 mice receiving repeated intravenous doses of ZIF-8@Que (50 mg/kg, once weekly for 4 weeks). (D) H&E staining of major organs confirming normal histology. Scale bar = 10 μm. (E) Experimental timeline for tumor establishment and treatment in nude mice. (F) Body weight of tumor-bearing mice during therapy. (G, H) Tumor growth curves (G) and tumor weight curves (H) for each group at different time points. (I) Kaplan-Meier survival curves for each group. (J) Representative tumor images at study endpoint. (K) H&E staining showing extensive necrosis in ZIF-8@Que-treated tumors. (L) Representative images of Ki67, cleaved caspase-1, cleaved caspase-3, cleaved GSDMD and TUNEL in tumor tissues, highlighting pyroptosis-mediated antitumor effects. For all studies, n ≥ 3. Data are shown as the mean ± SD. Comparisons were performed using the student's t-test or ANOVA. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, or ns = not significant.

    Techniques Used: In Vivo, Drug discovery, Hemolysis Assay, Incubation, Staining, TUNEL Assay



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    MedChemExpress cleaved caspase 1
    Schematic illustration of the mechanism of ZIF-8@Que nanoparticles in GC treatment. ZIF-8@Que nanoparticles were prepared via a one-pot co-precipitation process, encapsulating quercetin within the ZIF-8 framework. Upon systemic administration, ZIF-8@Que preferentially accumulates in gastric tumors and undergoes acidic pH-triggered drug release. The nanoparticles exhibit intrinsic POD-like activity, catalyzing H 2 O 2 to generate ROS, which disrupt mitochondrial function by collapsing Δψm, depleting ATP, and enhancing oxidative stress. ROS-driven mitochondrial injury subsequently activates inflammasome-dependent <t>caspase-1,</t> leading to GSDMD cleavage, pore formation, release of IL-1β and IL-18, and subsequent pyroptotic cell death. This cascade culminates in robust eradication of GC cells while sparing normal tissues, highlighting the therapeutic promise of ZIF-8@Que as pyroptosis-inducing nanoparticles.
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    Schematic illustration of the mechanism of ZIF-8@Que nanoparticles in GC treatment. ZIF-8@Que nanoparticles were prepared via a one-pot co-precipitation process, encapsulating quercetin within the ZIF-8 framework. Upon systemic administration, ZIF-8@Que preferentially accumulates in gastric tumors and undergoes acidic pH-triggered drug release. The nanoparticles exhibit intrinsic POD-like activity, catalyzing H 2 O 2 to generate ROS, which disrupt mitochondrial function by collapsing Δψm, depleting ATP, and enhancing oxidative stress. ROS-driven mitochondrial injury subsequently activates inflammasome-dependent <t>caspase-1,</t> leading to GSDMD cleavage, pore formation, release of IL-1β and IL-18, and subsequent pyroptotic cell death. This cascade culminates in robust eradication of GC cells while sparing normal tissues, highlighting the therapeutic promise of ZIF-8@Que as pyroptosis-inducing nanoparticles.
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    Schematic illustration of the mechanism of ZIF-8@Que nanoparticles in GC treatment. ZIF-8@Que nanoparticles were prepared via a one-pot co-precipitation process, encapsulating quercetin within the ZIF-8 framework. Upon systemic administration, ZIF-8@Que preferentially accumulates in gastric tumors and undergoes acidic pH-triggered drug release. The nanoparticles exhibit intrinsic POD-like activity, catalyzing H 2 O 2 to generate ROS, which disrupt mitochondrial function by collapsing Δψm, depleting ATP, and enhancing oxidative stress. ROS-driven mitochondrial injury subsequently activates inflammasome-dependent <t>caspase-1,</t> leading to GSDMD cleavage, pore formation, release of IL-1β and IL-18, and subsequent pyroptotic cell death. This cascade culminates in robust eradication of GC cells while sparing normal tissues, highlighting the therapeutic promise of ZIF-8@Que as pyroptosis-inducing nanoparticles.
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    Schematic illustration of the mechanism of ZIF-8@Que nanoparticles in GC treatment. ZIF-8@Que nanoparticles were prepared via a one-pot co-precipitation process, encapsulating quercetin within the ZIF-8 framework. Upon systemic administration, ZIF-8@Que preferentially accumulates in gastric tumors and undergoes acidic pH-triggered drug release. The nanoparticles exhibit intrinsic POD-like activity, catalyzing H 2 O 2 to generate ROS, which disrupt mitochondrial function by collapsing Δψm, depleting ATP, and enhancing oxidative stress. ROS-driven mitochondrial injury subsequently activates inflammasome-dependent <t>caspase-1,</t> leading to GSDMD cleavage, pore formation, release of IL-1β and IL-18, and subsequent pyroptotic cell death. This cascade culminates in robust eradication of GC cells while sparing normal tissues, highlighting the therapeutic promise of ZIF-8@Que as pyroptosis-inducing nanoparticles.
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    Differences in pyroptosis induced by COM crystals of different sizes (A) <t>Caspase-1/PI</t> double staining flow cytometry quantitative analysis. (B) Caspase-1/PI/Hoechst 33342 triple staining confocal observation. Scale bars, 50 μm. (C) NLRP3 immunofluorescence map. Scale bars, 100 μm. (D) Quantitative histogram of pyroptosis; n = 3; mean ± SEM. (E) Quantitative bar graph of NLRP3; n = 3; mean ± SEM. NC: normal control. COM crystals were incubated with HK-2 cells for 48 h. Compared with NC group, ∗ p < 0.05; ∗∗ p < 0.01. (A) flow graph is divided into four regions (Q1, Q2, Q3, and Q4), of which Q1 is PI high signal area and Caspase-1 low signal area, representing apoptotic necrotic cells. Q2 is the PI high signal region and Caspase-1 high signal region, which represents the late pyroptosis cells. Q3 is the PI low signal area and Caspase-1 high signal area, which represents the early pyroptosis cells (Caspase-1 is actively expressed). Q4 is the PI hypointense region and Caspase-1 hypointense region, representing normal cells. Q1+ Q2 refers to dead cells, and Q2+ Q3 refers to pyroptosis cells. (B) shows the presence of four types of cells: the first type is the normal cell (indicated by the orange arrow), which corresponds to the Q4 region cells in (A); the second type was apoptotic or necrotic cells (indicated by white arrow), namely Q1 region cells. The third type was the late pyroptosis cells (yellow arrow), which were Q2 cells. The fourth type is the cells in the early stage of pyroptosis (purple arrow), which is the Q3 region cells. Orange arrows refer to normal cells, white arrows to apoptotic necrotic cells, yellow arrows to late pyroptosis cells, and purple arrows to early pyroptosis cells.
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    Image Search Results


    Schematic illustration of the mechanism of ZIF-8@Que nanoparticles in GC treatment. ZIF-8@Que nanoparticles were prepared via a one-pot co-precipitation process, encapsulating quercetin within the ZIF-8 framework. Upon systemic administration, ZIF-8@Que preferentially accumulates in gastric tumors and undergoes acidic pH-triggered drug release. The nanoparticles exhibit intrinsic POD-like activity, catalyzing H 2 O 2 to generate ROS, which disrupt mitochondrial function by collapsing Δψm, depleting ATP, and enhancing oxidative stress. ROS-driven mitochondrial injury subsequently activates inflammasome-dependent caspase-1, leading to GSDMD cleavage, pore formation, release of IL-1β and IL-18, and subsequent pyroptotic cell death. This cascade culminates in robust eradication of GC cells while sparing normal tissues, highlighting the therapeutic promise of ZIF-8@Que as pyroptosis-inducing nanoparticles.

    Journal: Materials Today Bio

    Article Title: pH-responsive ZIF-8@quercetin nanoparticles induce pyroptosis for targeted gastric cancer therapy

    doi: 10.1016/j.mtbio.2026.102806

    Figure Lengend Snippet: Schematic illustration of the mechanism of ZIF-8@Que nanoparticles in GC treatment. ZIF-8@Que nanoparticles were prepared via a one-pot co-precipitation process, encapsulating quercetin within the ZIF-8 framework. Upon systemic administration, ZIF-8@Que preferentially accumulates in gastric tumors and undergoes acidic pH-triggered drug release. The nanoparticles exhibit intrinsic POD-like activity, catalyzing H 2 O 2 to generate ROS, which disrupt mitochondrial function by collapsing Δψm, depleting ATP, and enhancing oxidative stress. ROS-driven mitochondrial injury subsequently activates inflammasome-dependent caspase-1, leading to GSDMD cleavage, pore formation, release of IL-1β and IL-18, and subsequent pyroptotic cell death. This cascade culminates in robust eradication of GC cells while sparing normal tissues, highlighting the therapeutic promise of ZIF-8@Que as pyroptosis-inducing nanoparticles.

    Article Snippet: Endogenous peroxidase was quenched with 3 % H 2 O 2 for 25 min. After blocking with 3 % BSA for 30 min, sections were incubated overnight at 4 °C with primary antibodies: Ki67 (1:500, CST), Cleaved caspase 3 (1:200, Abcam), Cleaved Caspase 1 (1:100, MCE), and Cleaved GSDMD (1:500, MCE).

    Techniques: Activity Assay

    In vivo therapeutic efficacy and safety profile of ZIF-8@Que. (A) Hemolysis assay of mouse RBCs incubated with ZIF-8@Que at various concentrations. (B, C) Assessment of systemic toxicity in healthy mice: body weight (B) and serum biochemical (C) of C57BL/6 mice receiving repeated intravenous doses of ZIF-8@Que (50 mg/kg, once weekly for 4 weeks). (D) H&E staining of major organs confirming normal histology. Scale bar = 10 μm. (E) Experimental timeline for tumor establishment and treatment in nude mice. (F) Body weight of tumor-bearing mice during therapy. (G, H) Tumor growth curves (G) and tumor weight curves (H) for each group at different time points. (I) Kaplan-Meier survival curves for each group. (J) Representative tumor images at study endpoint. (K) H&E staining showing extensive necrosis in ZIF-8@Que-treated tumors. (L) Representative images of Ki67, cleaved caspase-1, cleaved caspase-3, cleaved GSDMD and TUNEL in tumor tissues, highlighting pyroptosis-mediated antitumor effects. For all studies, n ≥ 3. Data are shown as the mean ± SD. Comparisons were performed using the student's t-test or ANOVA. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, or ns = not significant.

    Journal: Materials Today Bio

    Article Title: pH-responsive ZIF-8@quercetin nanoparticles induce pyroptosis for targeted gastric cancer therapy

    doi: 10.1016/j.mtbio.2026.102806

    Figure Lengend Snippet: In vivo therapeutic efficacy and safety profile of ZIF-8@Que. (A) Hemolysis assay of mouse RBCs incubated with ZIF-8@Que at various concentrations. (B, C) Assessment of systemic toxicity in healthy mice: body weight (B) and serum biochemical (C) of C57BL/6 mice receiving repeated intravenous doses of ZIF-8@Que (50 mg/kg, once weekly for 4 weeks). (D) H&E staining of major organs confirming normal histology. Scale bar = 10 μm. (E) Experimental timeline for tumor establishment and treatment in nude mice. (F) Body weight of tumor-bearing mice during therapy. (G, H) Tumor growth curves (G) and tumor weight curves (H) for each group at different time points. (I) Kaplan-Meier survival curves for each group. (J) Representative tumor images at study endpoint. (K) H&E staining showing extensive necrosis in ZIF-8@Que-treated tumors. (L) Representative images of Ki67, cleaved caspase-1, cleaved caspase-3, cleaved GSDMD and TUNEL in tumor tissues, highlighting pyroptosis-mediated antitumor effects. For all studies, n ≥ 3. Data are shown as the mean ± SD. Comparisons were performed using the student's t-test or ANOVA. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, or ns = not significant.

    Article Snippet: Endogenous peroxidase was quenched with 3 % H 2 O 2 for 25 min. After blocking with 3 % BSA for 30 min, sections were incubated overnight at 4 °C with primary antibodies: Ki67 (1:500, CST), Cleaved caspase 3 (1:200, Abcam), Cleaved Caspase 1 (1:100, MCE), and Cleaved GSDMD (1:500, MCE).

    Techniques: In Vivo, Drug discovery, Hemolysis Assay, Incubation, Staining, TUNEL Assay

    Differences in pyroptosis induced by COM crystals of different sizes (A) Caspase-1/PI double staining flow cytometry quantitative analysis. (B) Caspase-1/PI/Hoechst 33342 triple staining confocal observation. Scale bars, 50 μm. (C) NLRP3 immunofluorescence map. Scale bars, 100 μm. (D) Quantitative histogram of pyroptosis; n = 3; mean ± SEM. (E) Quantitative bar graph of NLRP3; n = 3; mean ± SEM. NC: normal control. COM crystals were incubated with HK-2 cells for 48 h. Compared with NC group, ∗ p < 0.05; ∗∗ p < 0.01. (A) flow graph is divided into four regions (Q1, Q2, Q3, and Q4), of which Q1 is PI high signal area and Caspase-1 low signal area, representing apoptotic necrotic cells. Q2 is the PI high signal region and Caspase-1 high signal region, which represents the late pyroptosis cells. Q3 is the PI low signal area and Caspase-1 high signal area, which represents the early pyroptosis cells (Caspase-1 is actively expressed). Q4 is the PI hypointense region and Caspase-1 hypointense region, representing normal cells. Q1+ Q2 refers to dead cells, and Q2+ Q3 refers to pyroptosis cells. (B) shows the presence of four types of cells: the first type is the normal cell (indicated by the orange arrow), which corresponds to the Q4 region cells in (A); the second type was apoptotic or necrotic cells (indicated by white arrow), namely Q1 region cells. The third type was the late pyroptosis cells (yellow arrow), which were Q2 cells. The fourth type is the cells in the early stage of pyroptosis (purple arrow), which is the Q3 region cells. Orange arrows refer to normal cells, white arrows to apoptotic necrotic cells, yellow arrows to late pyroptosis cells, and purple arrows to early pyroptosis cells.

    Journal: iScience

    Article Title: Size-dependent pyroptosis induction by calcium oxalate monohydrate crystals in HK-2 cells

    doi: 10.1016/j.isci.2025.114459

    Figure Lengend Snippet: Differences in pyroptosis induced by COM crystals of different sizes (A) Caspase-1/PI double staining flow cytometry quantitative analysis. (B) Caspase-1/PI/Hoechst 33342 triple staining confocal observation. Scale bars, 50 μm. (C) NLRP3 immunofluorescence map. Scale bars, 100 μm. (D) Quantitative histogram of pyroptosis; n = 3; mean ± SEM. (E) Quantitative bar graph of NLRP3; n = 3; mean ± SEM. NC: normal control. COM crystals were incubated with HK-2 cells for 48 h. Compared with NC group, ∗ p < 0.05; ∗∗ p < 0.01. (A) flow graph is divided into four regions (Q1, Q2, Q3, and Q4), of which Q1 is PI high signal area and Caspase-1 low signal area, representing apoptotic necrotic cells. Q2 is the PI high signal region and Caspase-1 high signal region, which represents the late pyroptosis cells. Q3 is the PI low signal area and Caspase-1 high signal area, which represents the early pyroptosis cells (Caspase-1 is actively expressed). Q4 is the PI hypointense region and Caspase-1 hypointense region, representing normal cells. Q1+ Q2 refers to dead cells, and Q2+ Q3 refers to pyroptosis cells. (B) shows the presence of four types of cells: the first type is the normal cell (indicated by the orange arrow), which corresponds to the Q4 region cells in (A); the second type was apoptotic or necrotic cells (indicated by white arrow), namely Q1 region cells. The third type was the late pyroptosis cells (yellow arrow), which were Q2 cells. The fourth type is the cells in the early stage of pyroptosis (purple arrow), which is the Q3 region cells. Orange arrows refer to normal cells, white arrows to apoptotic necrotic cells, yellow arrows to late pyroptosis cells, and purple arrows to early pyroptosis cells.

    Article Snippet: Cleaved caspase-1 p20 , Proteintech , Cat No. 22915-1-AP; RRID: AB_2876874.

    Techniques: Double Staining, Flow Cytometry, Staining, Immunofluorescence, Control, Incubation

    Level of proteins in pyroptosis signaling pathway induced by COM crystals of different sizes (A) protein bands of NLRP3, cleaved caspase-1 p20, IL-18, and IL-1β. (B–E) Quantitative analysis of NLRP3, cleaved caspase-1 p20, IL-18, and IL-1β, respectively. n = 3; mean ± SEM. NC: normal control. COM crystals were incubated with HK-2 cells for 48 h.∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001.

    Journal: iScience

    Article Title: Size-dependent pyroptosis induction by calcium oxalate monohydrate crystals in HK-2 cells

    doi: 10.1016/j.isci.2025.114459

    Figure Lengend Snippet: Level of proteins in pyroptosis signaling pathway induced by COM crystals of different sizes (A) protein bands of NLRP3, cleaved caspase-1 p20, IL-18, and IL-1β. (B–E) Quantitative analysis of NLRP3, cleaved caspase-1 p20, IL-18, and IL-1β, respectively. n = 3; mean ± SEM. NC: normal control. COM crystals were incubated with HK-2 cells for 48 h.∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001.

    Article Snippet: Cleaved caspase-1 p20 , Proteintech , Cat No. 22915-1-AP; RRID: AB_2876874.

    Techniques: Control, Incubation