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human microglia primary cell culture complete media with serum  (Celprogen Inc)


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    Celprogen Inc human microglia primary cell culture complete media with serum
    Human Microglia Primary Cell Culture Complete Media With Serum, 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
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    Average 92 stars, based on 8 article reviews
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    human microglia primary cell culture complete media with serum  (Celprogen Inc)
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    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.
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    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.
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    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.
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    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.
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    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.
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    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.
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    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: