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cat  (MedChemExpress)


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  • 95

    Structured Review

    MedChemExpress cat

    Cat, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 95/100, based on 59 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/hy-p0151/SN50/pmc10830855-41-4-2
    Average 95 stars, based on 59 article reviews
    cat - by Bioz Stars, 2026-10
    95/100 stars

    Images

    1) Product Images from "Whitening of brown adipose tissue inhibits osteogenic differentiation via secretion of S100A8/A9"

    Article Title: Whitening of brown adipose tissue inhibits osteogenic differentiation via secretion of S100A8/A9

    Journal: iScience

    doi: 10.1016/j.isci.2024.108857


    Figure Legend Snippet:

    Techniques Used: Virus, Negative Control, Recombinant, Staining, Silver Staining, Enzyme-linked Immunosorbent Assay, CCK-8 Assay, Real-time Polymerase Chain Reaction, Software

    Related Articles

    other:

    Article Title: Pentraxin 3 ameliorates glucocorticoid-induced osteonecrosis of the femoral head via TLR4/NF-κB/FGF21 signaling axis
    Article Snippet: Regarding the concentrations of all drugs, the details are as follows: rPTX3: 200 ng/mL; rFGF21 (MCE, HY- P70473 , USA): 10 nM; ATF3 inducer 1: 50 μM; TAK-242 (MCE, HY-11109): 50 nM; SN50 (MCE, HY-P0151): 50 μg/mL.

    Multiple Displacement Amplification:

    Article Title: Curcumin and Glycyrrhiza glabra Synergistically Attenuate Alzheimer's Pathology via TLR4/NF-κB-Mediated Anti-inflammatory and Redox Modulation in a D-Gal/Sodium Nitrite-Induced Mouse Model.
    Article Snippet: Alzheimer’s disease (AD) is a progressive neurodegenerative disorder characterized by memory loss, cognitive decline, and behavioral abnormalities.. Pathologically, AD involves β-amyloid deposition, hyperphosphorylated tau protein, oxidative stress, and neuroinflammation, collectively contributing to neuronal damage and synaptic dysfunction [1, 2].. Notably, chronic activation of microglia and astrocytes via the Toll-like receptor 4 (TLR4)/NF-κB signaling cascade is considered a key driver of sustained neuroinflammatory responses in AD progression [3, 4].

    Real-time Polymerase Chain Reaction:

    Article Title: Curcumin and Glycyrrhiza glabra Synergistically Attenuate Alzheimer's Pathology via TLR4/NF-κB-Mediated Anti-inflammatory and Redox Modulation in a D-Gal/Sodium Nitrite-Induced Mouse Model.
    Article Snippet: Alzheimer’s disease (AD) is a progressive neurodegenerative disorder characterized by memory loss, cognitive decline, and behavioral abnormalities.. Pathologically, AD involves β-amyloid deposition, hyperphosphorylated tau protein, oxidative stress, and neuroinflammation, collectively contributing to neuronal damage and synaptic dysfunction [1, 2].. Notably, chronic activation of microglia and astrocytes via the Toll-like receptor 4 (TLR4)/NF-κB signaling cascade is considered a key driver of sustained neuroinflammatory responses in AD progression [3, 4].

    Marker:

    Article Title: Curcumin and Glycyrrhiza glabra Synergistically Attenuate Alzheimer's Pathology via TLR4/NF-κB-Mediated Anti-inflammatory and Redox Modulation in a D-Gal/Sodium Nitrite-Induced Mouse Model.
    Article Snippet: Alzheimer’s disease (AD) is a progressive neurodegenerative disorder characterized by memory loss, cognitive decline, and behavioral abnormalities.. Pathologically, AD involves β-amyloid deposition, hyperphosphorylated tau protein, oxidative stress, and neuroinflammation, collectively contributing to neuronal damage and synaptic dysfunction [1, 2].. Notably, chronic activation of microglia and astrocytes via the Toll-like receptor 4 (TLR4)/NF-κB signaling cascade is considered a key driver of sustained neuroinflammatory responses in AD progression [3, 4].

    Bicinchoninic Acid Protein Assay:

    Article Title: Curcumin and Glycyrrhiza glabra Synergistically Attenuate Alzheimer's Pathology via TLR4/NF-κB-Mediated Anti-inflammatory and Redox Modulation in a D-Gal/Sodium Nitrite-Induced Mouse Model.
    Article Snippet: Alzheimer’s disease (AD) is a progressive neurodegenerative disorder characterized by memory loss, cognitive decline, and behavioral abnormalities.. Pathologically, AD involves β-amyloid deposition, hyperphosphorylated tau protein, oxidative stress, and neuroinflammation, collectively contributing to neuronal damage and synaptic dysfunction [1, 2].. Notably, chronic activation of microglia and astrocytes via the Toll-like receptor 4 (TLR4)/NF-κB signaling cascade is considered a key driver of sustained neuroinflammatory responses in AD progression [3, 4].

    ATP Assay:

    Article Title: Selenomethionine regulates macrophage polarization through mitochondrial dynamics via NF-κB signaling to attenuate sepsis-induced cardiomyopathy.
    Article Snippet: .. Lipopolysaccharide (LPS; HY-D1056), selenomethionine (SeMet; 26046-90-2), JC-1 Assay Kit (HY-K0601), ATP Assay Kit (HY-K0314), hyaluronidase (HY-108903A), DNase I (HY-108882), clodronate liposomes (HY-172202), BAY 11-7082(HY-13453), and SN50 (HY-P0151) were obtained from MedChemExpress. .. MitoSO Red (S0061S) was purchased from Beyotime Biotechnology.

    Liposomes:

    Article Title: Selenomethionine regulates macrophage polarization through mitochondrial dynamics via NF-κB signaling to attenuate sepsis-induced cardiomyopathy.
    Article Snippet: .. Lipopolysaccharide (LPS; HY-D1056), selenomethionine (SeMet; 26046-90-2), JC-1 Assay Kit (HY-K0601), ATP Assay Kit (HY-K0314), hyaluronidase (HY-108903A), DNase I (HY-108882), clodronate liposomes (HY-172202), BAY 11-7082(HY-13453), and SN50 (HY-P0151) were obtained from MedChemExpress. .. MitoSO Red (S0061S) was purchased from Beyotime Biotechnology.



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    MedChemExpress additional intraperitoneal administrations
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    Image Search Results


    Increased IL-1β secretion by macrophages due to autophagy impairment enhances inflammatory chemokine expression in LSECs. ( A ) Protein expression in ATG7-KO macrophages and NC macrophages generated using the CRISPR-CAS9 system. ( B ) Evaluation of IL-1β and caspase-1 levels in the culture supernatant of THP-1 macrophages by ELISA following 24-hour stimulation with or without 25 ng/mL LPS (n = 3/group). ( C ) Experimental method using LPS-stimulated THP-1 macrophage conditioned medium. ( D ) Evaluation of NF-κB or MAP kinase-related proteins in TMNK-1 cells. ( E and F ) Inflammatory chemokine gene expression in TMNK-1 cells when treated with control medium or THP-1 macrophage conditioned medium (n = 4/group). SN50, NF-κB inhibitor; SP600125, JNK inhibitor; SB203580, p38 MAPK inhibitor. ( G ) Inflammatory chemokine gene expression measured 24 hours after treating TMNK-1 cells with varying concentrations of human recombinant IL-1β (n = 4/group). ( H ) Evaluation of inflammatory chemokine expression in TMNK-1 cells after 6 hours of stimulation with recombinant human IL-1β (5 ng/mL) in the presence of SP600125 and SB203580 (n = 4/group).

    Journal: Cellular and Molecular Gastroenterology and Hepatology

    Article Title: Liver Sinusoidal Endothelial Cells Promote Metabolic Dysfunction-associated Steatohepatitis Progression via Interleukin-1R1-mediated Chemokine Production Induced by Macrophage-derived Interleukin-1β

    doi: 10.1016/j.jcmgh.2025.101698

    Figure Lengend Snippet: Increased IL-1β secretion by macrophages due to autophagy impairment enhances inflammatory chemokine expression in LSECs. ( A ) Protein expression in ATG7-KO macrophages and NC macrophages generated using the CRISPR-CAS9 system. ( B ) Evaluation of IL-1β and caspase-1 levels in the culture supernatant of THP-1 macrophages by ELISA following 24-hour stimulation with or without 25 ng/mL LPS (n = 3/group). ( C ) Experimental method using LPS-stimulated THP-1 macrophage conditioned medium. ( D ) Evaluation of NF-κB or MAP kinase-related proteins in TMNK-1 cells. ( E and F ) Inflammatory chemokine gene expression in TMNK-1 cells when treated with control medium or THP-1 macrophage conditioned medium (n = 4/group). SN50, NF-κB inhibitor; SP600125, JNK inhibitor; SB203580, p38 MAPK inhibitor. ( G ) Inflammatory chemokine gene expression measured 24 hours after treating TMNK-1 cells with varying concentrations of human recombinant IL-1β (n = 4/group). ( H ) Evaluation of inflammatory chemokine expression in TMNK-1 cells after 6 hours of stimulation with recombinant human IL-1β (5 ng/mL) in the presence of SP600125 and SB203580 (n = 4/group).

    Article Snippet: The inhibitors used were as follows: the NF-κB inhibitor SN50 (HY-P0151; MedChemExpress), the JNK inhibitor SP600125 (HY-12041; MedChemExpress), the p38 MAPK inhibitor SB 203580 (HY-10256; MedChemExpress), and the IL-1R antagonist (IL-1Ra) (093-05991; FUJIFILM Wako Pure Chemical Corporation).

    Techniques: Expressing, Generated, CRISPR, Enzyme-linked Immunosorbent Assay, Gene Expression, Control, Recombinant

    Macrophage-derived IL-1β increases CCL2 expression in HSCs via JNK activation. ( A ) Evaluation of the levels of NF-κB or MAPK-related proteins in LX-2 cells. ( B, C ) CCL2 gene expression in LX-2 cells treated with the control medium or THP-1 macrophage conditioned medium (n = 3/group). SN50, NF-κB inhibitor; SP600125, JNK inhibitor; SB203580, p38 MAPK inhibitor. ( D ) Evaluation of CCL2 expression in TMNK-1 cells after 48 hours of stimulation with recombinant human IL-1β (5 ng/mL) in the presence of SP600125 and SB203580 (n = 4/group).

    Journal: Cellular and Molecular Gastroenterology and Hepatology

    Article Title: Liver Sinusoidal Endothelial Cells Promote Metabolic Dysfunction-associated Steatohepatitis Progression via Interleukin-1R1-mediated Chemokine Production Induced by Macrophage-derived Interleukin-1β

    doi: 10.1016/j.jcmgh.2025.101698

    Figure Lengend Snippet: Macrophage-derived IL-1β increases CCL2 expression in HSCs via JNK activation. ( A ) Evaluation of the levels of NF-κB or MAPK-related proteins in LX-2 cells. ( B, C ) CCL2 gene expression in LX-2 cells treated with the control medium or THP-1 macrophage conditioned medium (n = 3/group). SN50, NF-κB inhibitor; SP600125, JNK inhibitor; SB203580, p38 MAPK inhibitor. ( D ) Evaluation of CCL2 expression in TMNK-1 cells after 48 hours of stimulation with recombinant human IL-1β (5 ng/mL) in the presence of SP600125 and SB203580 (n = 4/group).

    Article Snippet: The inhibitors used were as follows: the NF-κB inhibitor SN50 (HY-P0151; MedChemExpress), the JNK inhibitor SP600125 (HY-12041; MedChemExpress), the p38 MAPK inhibitor SB 203580 (HY-10256; MedChemExpress), and the IL-1R antagonist (IL-1Ra) (093-05991; FUJIFILM Wako Pure Chemical Corporation).

    Techniques: Derivative Assay, Expressing, Activation Assay, Gene Expression, Control, Recombinant