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stat3 inhibitor cucurbitacin i  (MedChemExpress)


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    Structured Review

    MedChemExpress stat3 inhibitor cucurbitacin i
    Fig. 2 LILRB4 expression level on dMDSCs was regulated by p-STAT-3 during T. gondii infection. a Analysis of the expression of <t>STAT3</t> and p-STAT3S727 in human dMDSCs with or without T. gondii infection. b Results of p-STAT3 expression in mouse dMDSCs of the uninfected and infected WT mice were detected by flow cytometry. c Expression levels of STAT3, p-STAT3S727 and LILRB4 in human dMDSCs treated with or without STAT3i during T. gondii infection were detected by Western blot. d, e Results of p-STAT3 and LILRB4 expression in mouse dMDSCs treated with or without JSI-124 during T. gondii infection were detected by flow cytometry. The data on human dMDSCs were identified by a paired t-test. The data on mouse dMDSCs were identified by the unpaired t-test. Asterisks indicate a significant difference at *p < 0.05 and **p < 0.01. FMO, fluorescence minus one; GAPDH, glyceraldehyde 3-phosphate dehydrogenase; INF, infected; JSI-124, the inhibitor of STAT3 in vivo; LILRB4, leukocyte immunoglobulin-like receptor B4; mRNA, messenger RNA; NC, negative control; p-STAT3, phosphorylated STAT3; STAT3, signal transducer and activator of transcription 3; STAT3i, the inhibitor of STAT3 in vitro; WT, wild type.
    Stat3 Inhibitor Cucurbitacin I, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 20 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/hy-n1405/Cucurbitacin+I/pm37461040-57-26-32
    Average 94 stars, based on 20 article reviews
    stat3 inhibitor cucurbitacin i - by Bioz Stars, 2026-10
    94/100 stars

    Images

    1) Product Images from "LILRB4 regulates the function of decidual MDSCs via the SHP-2/STAT6 pathway during Toxoplasma gondii infection."

    Article Title: LILRB4 regulates the function of decidual MDSCs via the SHP-2/STAT6 pathway during Toxoplasma gondii infection.

    Journal: Parasites & vectors

    doi: 10.1186/s13071-023-05856-4

    Fig. 2 LILRB4 expression level on dMDSCs was regulated by p-STAT-3 during T. gondii infection. a Analysis of the expression of STAT3 and p-STAT3S727 in human dMDSCs with or without T. gondii infection. b Results of p-STAT3 expression in mouse dMDSCs of the uninfected and infected WT mice were detected by flow cytometry. c Expression levels of STAT3, p-STAT3S727 and LILRB4 in human dMDSCs treated with or without STAT3i during T. gondii infection were detected by Western blot. d, e Results of p-STAT3 and LILRB4 expression in mouse dMDSCs treated with or without JSI-124 during T. gondii infection were detected by flow cytometry. The data on human dMDSCs were identified by a paired t-test. The data on mouse dMDSCs were identified by the unpaired t-test. Asterisks indicate a significant difference at *p < 0.05 and **p < 0.01. FMO, fluorescence minus one; GAPDH, glyceraldehyde 3-phosphate dehydrogenase; INF, infected; JSI-124, the inhibitor of STAT3 in vivo; LILRB4, leukocyte immunoglobulin-like receptor B4; mRNA, messenger RNA; NC, negative control; p-STAT3, phosphorylated STAT3; STAT3, signal transducer and activator of transcription 3; STAT3i, the inhibitor of STAT3 in vitro; WT, wild type.
    Figure Legend Snippet: Fig. 2 LILRB4 expression level on dMDSCs was regulated by p-STAT-3 during T. gondii infection. a Analysis of the expression of STAT3 and p-STAT3S727 in human dMDSCs with or without T. gondii infection. b Results of p-STAT3 expression in mouse dMDSCs of the uninfected and infected WT mice were detected by flow cytometry. c Expression levels of STAT3, p-STAT3S727 and LILRB4 in human dMDSCs treated with or without STAT3i during T. gondii infection were detected by Western blot. d, e Results of p-STAT3 and LILRB4 expression in mouse dMDSCs treated with or without JSI-124 during T. gondii infection were detected by flow cytometry. The data on human dMDSCs were identified by a paired t-test. The data on mouse dMDSCs were identified by the unpaired t-test. Asterisks indicate a significant difference at *p < 0.05 and **p < 0.01. FMO, fluorescence minus one; GAPDH, glyceraldehyde 3-phosphate dehydrogenase; INF, infected; JSI-124, the inhibitor of STAT3 in vivo; LILRB4, leukocyte immunoglobulin-like receptor B4; mRNA, messenger RNA; NC, negative control; p-STAT3, phosphorylated STAT3; STAT3, signal transducer and activator of transcription 3; STAT3i, the inhibitor of STAT3 in vitro; WT, wild type.

    Techniques Used: Expressing, Infection, Flow Cytometry, Western Blot, Fluorescence, In Vivo, Negative Control, In Vitro

    Fig. 5 Diagrammatic representation of LILRB4 downregulation induced by T. gondii infection resulting in the dysfunction of dMDSCs. The phosphorylation level of STAT3 was decreased after T. gondii infection, resulting in the downregulation of LILRB4 on dMDSCs. The decreased level of LILRB4 reduced the phosphorylation of SHP-2 and then inhibited the activity of STAT6, which in turn inhibited the expression levels of Arg-1 and IL-10 via binding to their respective promoter during T. gondii infection. Arg-1, arginase-1; ARG1, the gene for Arg-1; dMDSCs, decidual myeloid-derived suppressor cells; Ig, immunoglobulin; IL-10, interleukin-10; IL10, the gene for IL-10; ITIM, immunoreceptor tyrosine-based inhibitory motifs; LILRB4, leukocyte immunoglobulin-like receptor B4; p-SHP2, phosphorylated SHP-2; p-STAT3, phosphorylated STAT3; p-STAT6, phosphorylated STAT6; SHP-2, src-homology 2 domain-containing protein tyrosine phosphatase; STAT3, signal transducer and activator of transcription 3; STAT6, signal transducer and activator of transcription 6.
    Figure Legend Snippet: Fig. 5 Diagrammatic representation of LILRB4 downregulation induced by T. gondii infection resulting in the dysfunction of dMDSCs. The phosphorylation level of STAT3 was decreased after T. gondii infection, resulting in the downregulation of LILRB4 on dMDSCs. The decreased level of LILRB4 reduced the phosphorylation of SHP-2 and then inhibited the activity of STAT6, which in turn inhibited the expression levels of Arg-1 and IL-10 via binding to their respective promoter during T. gondii infection. Arg-1, arginase-1; ARG1, the gene for Arg-1; dMDSCs, decidual myeloid-derived suppressor cells; Ig, immunoglobulin; IL-10, interleukin-10; IL10, the gene for IL-10; ITIM, immunoreceptor tyrosine-based inhibitory motifs; LILRB4, leukocyte immunoglobulin-like receptor B4; p-SHP2, phosphorylated SHP-2; p-STAT3, phosphorylated STAT3; p-STAT6, phosphorylated STAT6; SHP-2, src-homology 2 domain-containing protein tyrosine phosphatase; STAT3, signal transducer and activator of transcription 3; STAT6, signal transducer and activator of transcription 6.

    Techniques Used: Infection, Phospho-proteomics, Activity Assay, Expressing, Binding Assay, Derivative Assay

    Related Articles

    Blocking Assay:

    Article Title: Photobiomodulation reduces spinal cord edema by decreasing the expression of AQP4 in the astrocytes of male spinal cord injury rats via the JAK2/STAT3 signaling pathway.
    Article Snippet: .. To block the JAK2-STAT3 pathway, astrocytes in the preliminary study were pretreated with cucurbitacin I (0.5 μM, obtained from MedChemExpress) for one hour. .. In the second experiment, astrocytes were pretreated with the AQP4 inhibitor TGN020 (10 μM, MedChemExpress) for 1 hour to suppress AQP4 expression.

    DCFH-DA Assay:

    Article Title: JAK2/STAT3-dependent regulation of MDM4/MDM2-p53 signaling in methotrexate-induced ferroptosis and nephrotoxicity.
    Article Snippet: Methotrexate (MTX), a cornerstone therapeutic agent for malignancies and autoimmune diseases, is clinically constrained by its severe nephrotoxic effects.. Although oxidative stress and apoptosis have been implicated in MTX-induced nephrotoxicity, the precise molecular mechanisms underlying this process remain incompletely characterized.. This study investigates ferroptosis as a novel pathological contributor to MTX-induced nephrotoxicity and evaluates therapeutic interventions targeting the JAK2/STAT3-MDM4/MDM2 signaling axis.

    Colorimetric Assay:

    Article Title: JAK2/STAT3-dependent regulation of MDM4/MDM2-p53 signaling in methotrexate-induced ferroptosis and nephrotoxicity.
    Article Snippet: Methotrexate (MTX), a cornerstone therapeutic agent for malignancies and autoimmune diseases, is clinically constrained by its severe nephrotoxic effects.. Although oxidative stress and apoptosis have been implicated in MTX-induced nephrotoxicity, the precise molecular mechanisms underlying this process remain incompletely characterized.. This study investigates ferroptosis as a novel pathological contributor to MTX-induced nephrotoxicity and evaluates therapeutic interventions targeting the JAK2/STAT3-MDM4/MDM2 signaling axis.

    Concentration Assay:

    Article Title: Therapeutic Potential of Cucurbitacin I in Colon Adenocarcinoma Is Mediated by Modulation of SDHA Expression.
    Article Snippet: Upon reaching ~80% confluence, cells were washed with phosphate- buffered saline (PBS: Solarbio, Shanghai, China), followed by passage or plating and digested with 0.25% trypsin (Gibco, BOS, USA). .. Cucurbitacin I (CuI, MCE, NJ, USA) was dissolved in dimethyl sulfoxide (DMSO: Solarbio, Shanghai, China) to prepare stock solutions, and treatment concentrations were adjusted to ensure a final DMSO concentration remained ≤ 0.1% control wells received an equivalent volume of DMSO without CuI. ..

    Control:

    Article Title: Therapeutic Potential of Cucurbitacin I in Colon Adenocarcinoma Is Mediated by Modulation of SDHA Expression.
    Article Snippet: Upon reaching ~80% confluence, cells were washed with phosphate- buffered saline (PBS: Solarbio, Shanghai, China), followed by passage or plating and digested with 0.25% trypsin (Gibco, BOS, USA). .. Cucurbitacin I (CuI, MCE, NJ, USA) was dissolved in dimethyl sulfoxide (DMSO: Solarbio, Shanghai, China) to prepare stock solutions, and treatment concentrations were adjusted to ensure a final DMSO concentration remained ≤ 0.1% control wells received an equivalent volume of DMSO without CuI. ..



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