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primary m2 microglia  (Celprogen Inc)


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    Celprogen Inc primary m2 microglia
    Role of microglial TNF-α in NAC-induced microglia mortality. ( A ) Experimental schedule. ( B , C ) Representative images and quantitative analyses of microglial TNF-α in the prefrontal cortex of C57BL/6J and TNF fl/fl Cx3cr1-Cre ER mice after saline or tamoxifen treatment. TNF-α and Iba-1 are shown in red and green, respectively. Scale bars, 100 μm. ( C ) The transcript levels of microglial Tnf in C57BL/6J mice and TNF fl/fl Cx3cr1-Cre ER mice with or without tamoxifen (Tamo) treatment (n = 6). ( D ) Representative images and quantitative analyses of microglia viability after 48 h of NAC (30 mM; i.p.) treatment in C57BL/6J (n = 4) and microglial TNF-α-deficient mice (n = 4) with tamoxifen treatment (TNFKO). * p < 0.05, vs. saline (Con; C57BL/6J). Scale bars, 250 μm. ( E ) Transcript levels of TNF in the SK-N-SH, U-87 MG, and human primary <t>M2</t> microglia (n = 4). ( F ) Representative images and quantitative analyses of human M2 primary microglial viability after 24 h of treatment with LPS (0 and 10 ng/mL), and different doses of NAC (0, 5, 10, 20, 30, and 60 mM) (n = 6). Scale bars, 250 μm. ( G ) NO x synthesis after treatment with LPS (0 and 10 ng/mL), and NAC (0, 5, 10, 20, 30, and 60 mM) in human primary M2 microglia after 24 h (n = 6). ** p < 0.01, vs. control (Con). All data are presented as MEAN ± SEM.
    Primary M2 Microglia, supplied by Celprogen Inc, used in various techniques. Bioz Stars score: 92/100, based on 8 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/primary m2 microglia/product/Celprogen Inc
    Average 92 stars, based on 8 article reviews
    primary m2 microglia - by Bioz Stars, 2026-02
    92/100 stars

    Images

    1) Product Images from "N-Acetylcysteine Suppresses Microglial Inflammation and Induces Mortality Dose-Dependently via Tumor Necrosis Factor-α Signaling"

    Article Title: N-Acetylcysteine Suppresses Microglial Inflammation and Induces Mortality Dose-Dependently via Tumor Necrosis Factor-α Signaling

    Journal: International Journal of Molecular Sciences

    doi: 10.3390/ijms24043798

    Role of microglial TNF-α in NAC-induced microglia mortality. ( A ) Experimental schedule. ( B , C ) Representative images and quantitative analyses of microglial TNF-α in the prefrontal cortex of C57BL/6J and TNF fl/fl Cx3cr1-Cre ER mice after saline or tamoxifen treatment. TNF-α and Iba-1 are shown in red and green, respectively. Scale bars, 100 μm. ( C ) The transcript levels of microglial Tnf in C57BL/6J mice and TNF fl/fl Cx3cr1-Cre ER mice with or without tamoxifen (Tamo) treatment (n = 6). ( D ) Representative images and quantitative analyses of microglia viability after 48 h of NAC (30 mM; i.p.) treatment in C57BL/6J (n = 4) and microglial TNF-α-deficient mice (n = 4) with tamoxifen treatment (TNFKO). * p < 0.05, vs. saline (Con; C57BL/6J). Scale bars, 250 μm. ( E ) Transcript levels of TNF in the SK-N-SH, U-87 MG, and human primary M2 microglia (n = 4). ( F ) Representative images and quantitative analyses of human M2 primary microglial viability after 24 h of treatment with LPS (0 and 10 ng/mL), and different doses of NAC (0, 5, 10, 20, 30, and 60 mM) (n = 6). Scale bars, 250 μm. ( G ) NO x synthesis after treatment with LPS (0 and 10 ng/mL), and NAC (0, 5, 10, 20, 30, and 60 mM) in human primary M2 microglia after 24 h (n = 6). ** p < 0.01, vs. control (Con). All data are presented as MEAN ± SEM.
    Figure Legend Snippet: Role of microglial TNF-α in NAC-induced microglia mortality. ( A ) Experimental schedule. ( B , C ) Representative images and quantitative analyses of microglial TNF-α in the prefrontal cortex of C57BL/6J and TNF fl/fl Cx3cr1-Cre ER mice after saline or tamoxifen treatment. TNF-α and Iba-1 are shown in red and green, respectively. Scale bars, 100 μm. ( C ) The transcript levels of microglial Tnf in C57BL/6J mice and TNF fl/fl Cx3cr1-Cre ER mice with or without tamoxifen (Tamo) treatment (n = 6). ( D ) Representative images and quantitative analyses of microglia viability after 48 h of NAC (30 mM; i.p.) treatment in C57BL/6J (n = 4) and microglial TNF-α-deficient mice (n = 4) with tamoxifen treatment (TNFKO). * p < 0.05, vs. saline (Con; C57BL/6J). Scale bars, 250 μm. ( E ) Transcript levels of TNF in the SK-N-SH, U-87 MG, and human primary M2 microglia (n = 4). ( F ) Representative images and quantitative analyses of human M2 primary microglial viability after 24 h of treatment with LPS (0 and 10 ng/mL), and different doses of NAC (0, 5, 10, 20, 30, and 60 mM) (n = 6). Scale bars, 250 μm. ( G ) NO x synthesis after treatment with LPS (0 and 10 ng/mL), and NAC (0, 5, 10, 20, 30, and 60 mM) in human primary M2 microglia after 24 h (n = 6). ** p < 0.01, vs. control (Con). All data are presented as MEAN ± SEM.

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    primary m2 microglia  (Celprogen Inc)
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    Celprogen Inc primary m2 microglia
    Role of microglial TNF-α in NAC-induced microglia mortality. ( A ) Experimental schedule. ( B , C ) Representative images and quantitative analyses of microglial TNF-α in the prefrontal cortex of C57BL/6J and TNF fl/fl Cx3cr1-Cre ER mice after saline or tamoxifen treatment. TNF-α and Iba-1 are shown in red and green, respectively. Scale bars, 100 μm. ( C ) The transcript levels of microglial Tnf in C57BL/6J mice and TNF fl/fl Cx3cr1-Cre ER mice with or without tamoxifen (Tamo) treatment (n = 6). ( D ) Representative images and quantitative analyses of microglia viability after 48 h of NAC (30 mM; i.p.) treatment in C57BL/6J (n = 4) and microglial TNF-α-deficient mice (n = 4) with tamoxifen treatment (TNFKO). * p < 0.05, vs. saline (Con; C57BL/6J). Scale bars, 250 μm. ( E ) Transcript levels of TNF in the SK-N-SH, U-87 MG, and human primary <t>M2</t> microglia (n = 4). ( F ) Representative images and quantitative analyses of human M2 primary microglial viability after 24 h of treatment with LPS (0 and 10 ng/mL), and different doses of NAC (0, 5, 10, 20, 30, and 60 mM) (n = 6). Scale bars, 250 μm. ( G ) NO x synthesis after treatment with LPS (0 and 10 ng/mL), and NAC (0, 5, 10, 20, 30, and 60 mM) in human primary M2 microglia after 24 h (n = 6). ** p < 0.01, vs. control (Con). All data are presented as MEAN ± SEM.
    Primary M2 Microglia, supplied by Celprogen Inc, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/primary m2 microglia/product/Celprogen Inc
    Average 92 stars, based on 1 article reviews
    primary m2 microglia - by Bioz Stars, 2026-02
    92/100 stars
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    human primary m2 microglia  (Celprogen Inc)
    94
    Celprogen Inc human primary m2 microglia
    Role of microglial TNF-α in <t>NAC-induced</t> <t>microglia</t> mortality. ( A ) Experimental schedule. ( B , C ) Representative images and quantitative analyses of microglial TNF-α in the prefrontal cortex of C57BL/6J and TNF fl/fl Cx3cr1-Cre ER mice after saline or tamoxifen treatment. TNF-α and Iba-1 are shown in red and green, respectively. Scale bars, 100 μm. ( C ) The transcript levels of microglial Tnf in C57BL/6J mice and TNF fl/fl Cx3cr1-Cre ER mice with or without tamoxifen (Tamo) treatment (n = 6). ( D ) Representative images and quantitative analyses of microglia viability after 48 h of NAC (30 mM; i.p.) treatment in C57BL/6J (n = 4) and microglial TNF-α-deficient mice (n = 4) with tamoxifen treatment (TNFKO). * p < 0.05, vs. saline (Con; C57BL/6J). Scale bars, 250 μm. ( E ) Transcript levels of TNF in the SK-N-SH, U-87 MG, and human primary <t>M2</t> microglia (n = 4). ( F ) Representative images and quantitative analyses of human M2 primary microglial viability after 24 h of treatment with LPS (0 and 10 ng/mL), and different doses of NAC (0, 5, 10, 20, 30, and 60 mM) (n = 6). Scale bars, 250 μm. ( G ) NO x synthesis after treatment with LPS (0 and 10 ng/mL), and NAC (0, 5, 10, 20, 30, and 60 mM) in human primary M2 microglia after 24 h (n = 6). ** p < 0.01, vs. control (Con). All data are presented as MEAN ± SEM.
    Human Primary M2 Microglia, supplied by Celprogen Inc, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/human primary m2 microglia/product/Celprogen Inc
    Average 94 stars, based on 1 article reviews
    human primary m2 microglia - by Bioz Stars, 2026-02
    94/100 stars
    		  Buy from Supplier

    Image Search Results


    Role of microglial TNF-α in NAC-induced microglia mortality. ( A ) Experimental schedule. ( B , C ) Representative images and quantitative analyses of microglial TNF-α in the prefrontal cortex of C57BL/6J and TNF fl/fl Cx3cr1-Cre ER mice after saline or tamoxifen treatment. TNF-α and Iba-1 are shown in red and green, respectively. Scale bars, 100 μm. ( C ) The transcript levels of microglial Tnf in C57BL/6J mice and TNF fl/fl Cx3cr1-Cre ER mice with or without tamoxifen (Tamo) treatment (n = 6). ( D ) Representative images and quantitative analyses of microglia viability after 48 h of NAC (30 mM; i.p.) treatment in C57BL/6J (n = 4) and microglial TNF-α-deficient mice (n = 4) with tamoxifen treatment (TNFKO). * p < 0.05, vs. saline (Con; C57BL/6J). Scale bars, 250 μm. ( E ) Transcript levels of TNF in the SK-N-SH, U-87 MG, and human primary M2 microglia (n = 4). ( F ) Representative images and quantitative analyses of human M2 primary microglial viability after 24 h of treatment with LPS (0 and 10 ng/mL), and different doses of NAC (0, 5, 10, 20, 30, and 60 mM) (n = 6). Scale bars, 250 μm. ( G ) NO x synthesis after treatment with LPS (0 and 10 ng/mL), and NAC (0, 5, 10, 20, 30, and 60 mM) in human primary M2 microglia after 24 h (n = 6). ** p < 0.01, vs. control (Con). All data are presented as MEAN ± SEM.

    Journal: International Journal of Molecular Sciences

    Article Title: N-Acetylcysteine Suppresses Microglial Inflammation and Induces Mortality Dose-Dependently via Tumor Necrosis Factor-α Signaling

    doi: 10.3390/ijms24043798

    Figure Lengend Snippet: Role of microglial TNF-α in NAC-induced microglia mortality. ( A ) Experimental schedule. ( B , C ) Representative images and quantitative analyses of microglial TNF-α in the prefrontal cortex of C57BL/6J and TNF fl/fl Cx3cr1-Cre ER mice after saline or tamoxifen treatment. TNF-α and Iba-1 are shown in red and green, respectively. Scale bars, 100 μm. ( C ) The transcript levels of microglial Tnf in C57BL/6J mice and TNF fl/fl Cx3cr1-Cre ER mice with or without tamoxifen (Tamo) treatment (n = 6). ( D ) Representative images and quantitative analyses of microglia viability after 48 h of NAC (30 mM; i.p.) treatment in C57BL/6J (n = 4) and microglial TNF-α-deficient mice (n = 4) with tamoxifen treatment (TNFKO). * p < 0.05, vs. saline (Con; C57BL/6J). Scale bars, 250 μm. ( E ) Transcript levels of TNF in the SK-N-SH, U-87 MG, and human primary M2 microglia (n = 4). ( F ) Representative images and quantitative analyses of human M2 primary microglial viability after 24 h of treatment with LPS (0 and 10 ng/mL), and different doses of NAC (0, 5, 10, 20, 30, and 60 mM) (n = 6). Scale bars, 250 μm. ( G ) NO x synthesis after treatment with LPS (0 and 10 ng/mL), and NAC (0, 5, 10, 20, 30, and 60 mM) in human primary M2 microglia after 24 h (n = 6). ** p < 0.01, vs. control (Con). All data are presented as MEAN ± SEM.

    Article Snippet: Media containing serum of human primary M2 microglia (CELPROGEN, SKU:M37089-01S) was changed every 3 days.

    Techniques:

    Role of microglial TNF-α in NAC-induced microglia mortality. ( A ) Experimental schedule. ( B , C ) Representative images and quantitative analyses of microglial TNF-α in the prefrontal cortex of C57BL/6J and TNF fl/fl Cx3cr1-Cre ER mice after saline or tamoxifen treatment. TNF-α and Iba-1 are shown in red and green, respectively. Scale bars, 100 μm. ( C ) The transcript levels of microglial Tnf in C57BL/6J mice and TNF fl/fl Cx3cr1-Cre ER mice with or without tamoxifen (Tamo) treatment (n = 6). ( D ) Representative images and quantitative analyses of microglia viability after 48 h of NAC (30 mM; i.p.) treatment in C57BL/6J (n = 4) and microglial TNF-α-deficient mice (n = 4) with tamoxifen treatment (TNFKO). * p < 0.05, vs. saline (Con; C57BL/6J). Scale bars, 250 μm. ( E ) Transcript levels of TNF in the SK-N-SH, U-87 MG, and human primary M2 microglia (n = 4). ( F ) Representative images and quantitative analyses of human M2 primary microglial viability after 24 h of treatment with LPS (0 and 10 ng/mL), and different doses of NAC (0, 5, 10, 20, 30, and 60 mM) (n = 6). Scale bars, 250 μm. ( G ) NO x synthesis after treatment with LPS (0 and 10 ng/mL), and NAC (0, 5, 10, 20, 30, and 60 mM) in human primary M2 microglia after 24 h (n = 6). ** p < 0.01, vs. control (Con). All data are presented as MEAN ± SEM.

    Journal: International Journal of Molecular Sciences

    Article Title: N-Acetylcysteine Suppresses Microglial Inflammation and Induces Mortality Dose-Dependently via Tumor Necrosis Factor-α Signaling

    doi: 10.3390/ijms24043798

    Figure Lengend Snippet: Role of microglial TNF-α in NAC-induced microglia mortality. ( A ) Experimental schedule. ( B , C ) Representative images and quantitative analyses of microglial TNF-α in the prefrontal cortex of C57BL/6J and TNF fl/fl Cx3cr1-Cre ER mice after saline or tamoxifen treatment. TNF-α and Iba-1 are shown in red and green, respectively. Scale bars, 100 μm. ( C ) The transcript levels of microglial Tnf in C57BL/6J mice and TNF fl/fl Cx3cr1-Cre ER mice with or without tamoxifen (Tamo) treatment (n = 6). ( D ) Representative images and quantitative analyses of microglia viability after 48 h of NAC (30 mM; i.p.) treatment in C57BL/6J (n = 4) and microglial TNF-α-deficient mice (n = 4) with tamoxifen treatment (TNFKO). * p < 0.05, vs. saline (Con; C57BL/6J). Scale bars, 250 μm. ( E ) Transcript levels of TNF in the SK-N-SH, U-87 MG, and human primary M2 microglia (n = 4). ( F ) Representative images and quantitative analyses of human M2 primary microglial viability after 24 h of treatment with LPS (0 and 10 ng/mL), and different doses of NAC (0, 5, 10, 20, 30, and 60 mM) (n = 6). Scale bars, 250 μm. ( G ) NO x synthesis after treatment with LPS (0 and 10 ng/mL), and NAC (0, 5, 10, 20, 30, and 60 mM) in human primary M2 microglia after 24 h (n = 6). ** p < 0.01, vs. control (Con). All data are presented as MEAN ± SEM.

    Article Snippet: Human primary M2 microglia from the cortex were purchased from CELPROGEN Inc. (SKU:37089-01; Torrance, CA, USA).

    Techniques: