passages 21 30  (ATCC)


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    ATCC passages 21 30
    Passages 21 30, supplied by ATCC, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    cells passages 21 24  (ATCC)


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    ATCC cells passages 21 24
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    passage 21  (ATCC)


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    ATCC passage 21
    Passage 21, supplied by ATCC, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    passage 21  (ATCC)


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    ATCC passage 21
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    passages 21 30  (ATCC)


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    ATCC passages 21 30
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    cls substrain 1 passage 21  (ATCC)


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    ATCC cls substrain 1 passage 21
    Cls Substrain 1 Passage 21, supplied by ATCC, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    passage 21 p 21 bend3 mouse cerebral endothelial cell line  (ATCC)


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    ATCC passage 21 p 21 bend3 mouse cerebral endothelial cell line
    ALP attenuated oAβ-induced calcium influx. (a) <t>bEND3</t> cells were incubated with the calcium indicator (2 μM Fluo-4, AM), pretreated with or without 20 nM ALP for 4 h, and then incubated with 5 μM oAβ or 1 μM A-23187 (a positive control) for 15 min. Normalized data are expressed as mean ± SE (***p < 0.001, comparing with control group; ○○○p < 0.001, comparing with 5 μM oAβ treatment only group) from four independent experiments (N = 4). (b) Representative Western blot images of L-type Ca2+ channel and β-actin in cells with different treatments.
    Passage 21 P 21 Bend3 Mouse Cerebral Endothelial Cell Line, supplied by ATCC, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "Azelnidipine Attenuates the Oxidative and NF κ B Pathways in Amyloid- β -Stimulated Cerebral Endothelial Cells"

    Article Title: Azelnidipine Attenuates the Oxidative and NF κ B Pathways in Amyloid- β -Stimulated Cerebral Endothelial Cells

    Journal: ACS chemical neuroscience

    doi: 10.1021/acschemneuro.8b00368

    ALP attenuated oAβ-induced calcium influx. (a) bEND3 cells were incubated with the calcium indicator (2 μM Fluo-4, AM), pretreated with or without 20 nM ALP for 4 h, and then incubated with 5 μM oAβ or 1 μM A-23187 (a positive control) for 15 min. Normalized data are expressed as mean ± SE (***p < 0.001, comparing with control group; ○○○p < 0.001, comparing with 5 μM oAβ treatment only group) from four independent experiments (N = 4). (b) Representative Western blot images of L-type Ca2+ channel and β-actin in cells with different treatments.
    Figure Legend Snippet: ALP attenuated oAβ-induced calcium influx. (a) bEND3 cells were incubated with the calcium indicator (2 μM Fluo-4, AM), pretreated with or without 20 nM ALP for 4 h, and then incubated with 5 μM oAβ or 1 μM A-23187 (a positive control) for 15 min. Normalized data are expressed as mean ± SE (***p < 0.001, comparing with control group; ○○○p < 0.001, comparing with 5 μM oAβ treatment only group) from four independent experiments (N = 4). (b) Representative Western blot images of L-type Ca2+ channel and β-actin in cells with different treatments.

    Techniques Used: Incubation, Positive Control, Western Blot

    ALP attenuated oAβ-induced phosphorylation of ERK p42 and p44. bEND3 cells were treated with 20 nM ALP for 4 h, and followed by treatment with or without 5 μM oAβ for 15 min. (a–c) Phospho- and total ERK p42/p44 and (d, e) phospho- and total p38 were quantified with Western blot analysis and expressed as ratio of phospho to total and as fraction percentages of the control group with the mean ± SD from four independent experiments (N = 4) (***p < 0.001, **p < 0.01, *p < 0.05 comparing with control group; ○○p < 0.01, ○p < 0.05 comparing with 5 μM oAβ treatment only group). (f, g) Representative Western blot images of total ERK p44/p42, p38, and β-actin.
    Figure Legend Snippet: ALP attenuated oAβ-induced phosphorylation of ERK p42 and p44. bEND3 cells were treated with 20 nM ALP for 4 h, and followed by treatment with or without 5 μM oAβ for 15 min. (a–c) Phospho- and total ERK p42/p44 and (d, e) phospho- and total p38 were quantified with Western blot analysis and expressed as ratio of phospho to total and as fraction percentages of the control group with the mean ± SD from four independent experiments (N = 4) (***p < 0.001, **p < 0.01, *p < 0.05 comparing with control group; ○○p < 0.01, ○p < 0.05 comparing with 5 μM oAβ treatment only group). (f, g) Representative Western blot images of total ERK p44/p42, p38, and β-actin.

    Techniques Used: Western Blot

    Azelnidipine attenuated oAβ-induced phosphorylation of cPLA2. bEND3 cells were treated with 20 nM ALP for 4 h, followed by treatment with or without 5 μM oAβ for 30 min. (a, b) Phospho- and total cPLA2 were quantified by Western blot analysis. Data are expressed as a ratio of phospho- to total protein and normalized by the control group with the mean ± SD from three independent experiments (N = 3) (***p < 0.001, comparing with control group; ○○○p < 0.001, comparing with 5 μM oAβ treatment only group). (c) Representative Western blot images of total cPLA2 and β-actin.
    Figure Legend Snippet: Azelnidipine attenuated oAβ-induced phosphorylation of cPLA2. bEND3 cells were treated with 20 nM ALP for 4 h, followed by treatment with or without 5 μM oAβ for 30 min. (a, b) Phospho- and total cPLA2 were quantified by Western blot analysis. Data are expressed as a ratio of phospho- to total protein and normalized by the control group with the mean ± SD from three independent experiments (N = 3) (***p < 0.001, comparing with control group; ○○○p < 0.001, comparing with 5 μM oAβ treatment only group). (c) Representative Western blot images of total cPLA2 and β-actin.

    Techniques Used: Western Blot

    Azelnidipine attenuated oAβ-induced superoxide anion production. bEND3 cells were treated with 20 nM ALP for 4 h, followed by treatment with or without 5 μM oAβ for 30 min. Superoxide anion production was quantified by measuring the DHE intensity within each sample. Data are normalized by the control group with the mean ± SD from three independent experiments (N = 3) (***p < 0.001, comparing with control group; ○○p < 0.01 comparing with 5 μM oAβ treatment only group).
    Figure Legend Snippet: Azelnidipine attenuated oAβ-induced superoxide anion production. bEND3 cells were treated with 20 nM ALP for 4 h, followed by treatment with or without 5 μM oAβ for 30 min. Superoxide anion production was quantified by measuring the DHE intensity within each sample. Data are normalized by the control group with the mean ± SD from three independent experiments (N = 3) (***p < 0.001, comparing with control group; ○○p < 0.01 comparing with 5 μM oAβ treatment only group).

    Techniques Used:

    Azelnidipine attenuated oAβ-induced NFκB activation. bEND3 cells were treated with 20 nM ALP, 5 μM Aβ, both ALP and Aβ, 10 μM MAFP, both MAFP and Aβ, 2 μM BEL, and both BEL and Aβ or 100 ng/mL TNFα (positive control) to yield a total of nine datasets. (a) Nucleus staining is represented in red, and NFκB p65 subunit in green immunofluorescence. The merged images were obtained by superposing the nucleus staining and NFκB p65 subunit in the same field acquired using different filter sets. (b) NFκB activation was quantified by the ratio of NFκB p65 subunit intensity in nuclei to that in cytoplasm. Data are expressed with the mean ± SD from four independent experiments reported (N = 4) (*p < 0.05, **p < 0.01, comparing with control group; ○p < 0.05, comparing with 5 μM oAβ treatment only group).
    Figure Legend Snippet: Azelnidipine attenuated oAβ-induced NFκB activation. bEND3 cells were treated with 20 nM ALP, 5 μM Aβ, both ALP and Aβ, 10 μM MAFP, both MAFP and Aβ, 2 μM BEL, and both BEL and Aβ or 100 ng/mL TNFα (positive control) to yield a total of nine datasets. (a) Nucleus staining is represented in red, and NFκB p65 subunit in green immunofluorescence. The merged images were obtained by superposing the nucleus staining and NFκB p65 subunit in the same field acquired using different filter sets. (b) NFκB activation was quantified by the ratio of NFκB p65 subunit intensity in nuclei to that in cytoplasm. Data are expressed with the mean ± SD from four independent experiments reported (N = 4) (*p < 0.05, **p < 0.01, comparing with control group; ○p < 0.05, comparing with 5 μM oAβ treatment only group).

    Techniques Used: Activation Assay, Positive Control, Staining, Immunofluorescence

    passage 21 p 21 bend3 mouse cerebral endothelial cell line  (ATCC)


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    ATCC passage 21 p 21 bend3 mouse cerebral endothelial cell line
    ALP attenuated oAβ-induced calcium influx. (a) <t>bEND3</t> cells were incubated with the calcium indicator (2 μM Fluo-4, AM), pretreated with or without 20 nM ALP for 4 h, and then incubated with 5 μM oAβ or 1 μM A-23187 (a positive control) for 15 min. Normalized data are expressed as mean ± SE (***p < 0.001, comparing with control group; ○○○p < 0.001, comparing with 5 μM oAβ treatment only group) from four independent experiments (N = 4). (b) Representative Western blot images of L-type Ca2+ channel and β-actin in cells with different treatments.
    Passage 21 P 21 Bend3 Mouse Cerebral Endothelial Cell Line, supplied by ATCC, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Images

    1) Product Images from "Azelnidipine Attenuates the Oxidative and NF κ B Pathways in Amyloid- β -Stimulated Cerebral Endothelial Cells"

    Article Title: Azelnidipine Attenuates the Oxidative and NF κ B Pathways in Amyloid- β -Stimulated Cerebral Endothelial Cells

    Journal: ACS chemical neuroscience

    doi: 10.1021/acschemneuro.8b00368

    ALP attenuated oAβ-induced calcium influx. (a) bEND3 cells were incubated with the calcium indicator (2 μM Fluo-4, AM), pretreated with or without 20 nM ALP for 4 h, and then incubated with 5 μM oAβ or 1 μM A-23187 (a positive control) for 15 min. Normalized data are expressed as mean ± SE (***p < 0.001, comparing with control group; ○○○p < 0.001, comparing with 5 μM oAβ treatment only group) from four independent experiments (N = 4). (b) Representative Western blot images of L-type Ca2+ channel and β-actin in cells with different treatments.
    Figure Legend Snippet: ALP attenuated oAβ-induced calcium influx. (a) bEND3 cells were incubated with the calcium indicator (2 μM Fluo-4, AM), pretreated with or without 20 nM ALP for 4 h, and then incubated with 5 μM oAβ or 1 μM A-23187 (a positive control) for 15 min. Normalized data are expressed as mean ± SE (***p < 0.001, comparing with control group; ○○○p < 0.001, comparing with 5 μM oAβ treatment only group) from four independent experiments (N = 4). (b) Representative Western blot images of L-type Ca2+ channel and β-actin in cells with different treatments.

    Techniques Used: Incubation, Positive Control, Western Blot

    ALP attenuated oAβ-induced phosphorylation of ERK p42 and p44. bEND3 cells were treated with 20 nM ALP for 4 h, and followed by treatment with or without 5 μM oAβ for 15 min. (a–c) Phospho- and total ERK p42/p44 and (d, e) phospho- and total p38 were quantified with Western blot analysis and expressed as ratio of phospho to total and as fraction percentages of the control group with the mean ± SD from four independent experiments (N = 4) (***p < 0.001, **p < 0.01, *p < 0.05 comparing with control group; ○○p < 0.01, ○p < 0.05 comparing with 5 μM oAβ treatment only group). (f, g) Representative Western blot images of total ERK p44/p42, p38, and β-actin.
    Figure Legend Snippet: ALP attenuated oAβ-induced phosphorylation of ERK p42 and p44. bEND3 cells were treated with 20 nM ALP for 4 h, and followed by treatment with or without 5 μM oAβ for 15 min. (a–c) Phospho- and total ERK p42/p44 and (d, e) phospho- and total p38 were quantified with Western blot analysis and expressed as ratio of phospho to total and as fraction percentages of the control group with the mean ± SD from four independent experiments (N = 4) (***p < 0.001, **p < 0.01, *p < 0.05 comparing with control group; ○○p < 0.01, ○p < 0.05 comparing with 5 μM oAβ treatment only group). (f, g) Representative Western blot images of total ERK p44/p42, p38, and β-actin.

    Techniques Used: Western Blot

    Azelnidipine attenuated oAβ-induced phosphorylation of cPLA2. bEND3 cells were treated with 20 nM ALP for 4 h, followed by treatment with or without 5 μM oAβ for 30 min. (a, b) Phospho- and total cPLA2 were quantified by Western blot analysis. Data are expressed as a ratio of phospho- to total protein and normalized by the control group with the mean ± SD from three independent experiments (N = 3) (***p < 0.001, comparing with control group; ○○○p < 0.001, comparing with 5 μM oAβ treatment only group). (c) Representative Western blot images of total cPLA2 and β-actin.
    Figure Legend Snippet: Azelnidipine attenuated oAβ-induced phosphorylation of cPLA2. bEND3 cells were treated with 20 nM ALP for 4 h, followed by treatment with or without 5 μM oAβ for 30 min. (a, b) Phospho- and total cPLA2 were quantified by Western blot analysis. Data are expressed as a ratio of phospho- to total protein and normalized by the control group with the mean ± SD from three independent experiments (N = 3) (***p < 0.001, comparing with control group; ○○○p < 0.001, comparing with 5 μM oAβ treatment only group). (c) Representative Western blot images of total cPLA2 and β-actin.

    Techniques Used: Western Blot

    Azelnidipine attenuated oAβ-induced superoxide anion production. bEND3 cells were treated with 20 nM ALP for 4 h, followed by treatment with or without 5 μM oAβ for 30 min. Superoxide anion production was quantified by measuring the DHE intensity within each sample. Data are normalized by the control group with the mean ± SD from three independent experiments (N = 3) (***p < 0.001, comparing with control group; ○○p < 0.01 comparing with 5 μM oAβ treatment only group).
    Figure Legend Snippet: Azelnidipine attenuated oAβ-induced superoxide anion production. bEND3 cells were treated with 20 nM ALP for 4 h, followed by treatment with or without 5 μM oAβ for 30 min. Superoxide anion production was quantified by measuring the DHE intensity within each sample. Data are normalized by the control group with the mean ± SD from three independent experiments (N = 3) (***p < 0.001, comparing with control group; ○○p < 0.01 comparing with 5 μM oAβ treatment only group).

    Techniques Used:

    Azelnidipine attenuated oAβ-induced NFκB activation. bEND3 cells were treated with 20 nM ALP, 5 μM Aβ, both ALP and Aβ, 10 μM MAFP, both MAFP and Aβ, 2 μM BEL, and both BEL and Aβ or 100 ng/mL TNFα (positive control) to yield a total of nine datasets. (a) Nucleus staining is represented in red, and NFκB p65 subunit in green immunofluorescence. The merged images were obtained by superposing the nucleus staining and NFκB p65 subunit in the same field acquired using different filter sets. (b) NFκB activation was quantified by the ratio of NFκB p65 subunit intensity in nuclei to that in cytoplasm. Data are expressed with the mean ± SD from four independent experiments reported (N = 4) (*p < 0.05, **p < 0.01, comparing with control group; ○p < 0.05, comparing with 5 μM oAβ treatment only group).
    Figure Legend Snippet: Azelnidipine attenuated oAβ-induced NFκB activation. bEND3 cells were treated with 20 nM ALP, 5 μM Aβ, both ALP and Aβ, 10 μM MAFP, both MAFP and Aβ, 2 μM BEL, and both BEL and Aβ or 100 ng/mL TNFα (positive control) to yield a total of nine datasets. (a) Nucleus staining is represented in red, and NFκB p65 subunit in green immunofluorescence. The merged images were obtained by superposing the nucleus staining and NFκB p65 subunit in the same field acquired using different filter sets. (b) NFκB activation was quantified by the ratio of NFκB p65 subunit intensity in nuclei to that in cytoplasm. Data are expressed with the mean ± SD from four independent experiments reported (N = 4) (*p < 0.05, **p < 0.01, comparing with control group; ○p < 0.05, comparing with 5 μM oAβ treatment only group).

    Techniques Used: Activation Assay, Positive Control, Staining, Immunofluorescence

    passage 21  (ATCC)


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    ATCC passage 21
    Passage 21, supplied by ATCC, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    passage 21  (ATCC)


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    ATCC passage 21
    Passage 21, supplied by ATCC, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    passage 19 21  (ATCC)


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    ATCC passage 19 21
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    ATCC passage 21 p 21 bend3 mouse cerebral endothelial cell line
    ALP attenuated oAβ-induced calcium influx. (a) <t>bEND3</t> cells were incubated with the calcium indicator (2 μM Fluo-4, AM), pretreated with or without 20 nM ALP for 4 h, and then incubated with 5 μM oAβ or 1 μM A-23187 (a positive control) for 15 min. Normalized data are expressed as mean ± SE (***p < 0.001, comparing with control group; ○○○p < 0.001, comparing with 5 μM oAβ treatment only group) from four independent experiments (N = 4). (b) Representative Western blot images of L-type Ca2+ channel and β-actin in cells with different treatments.
    Passage 21 P 21 Bend3 Mouse Cerebral Endothelial Cell Line, supplied by ATCC, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    ATCC passage 19 21
    ALP attenuated oAβ-induced calcium influx. (a) <t>bEND3</t> cells were incubated with the calcium indicator (2 μM Fluo-4, AM), pretreated with or without 20 nM ALP for 4 h, and then incubated with 5 μM oAβ or 1 μM A-23187 (a positive control) for 15 min. Normalized data are expressed as mean ± SE (***p < 0.001, comparing with control group; ○○○p < 0.001, comparing with 5 μM oAβ treatment only group) from four independent experiments (N = 4). (b) Representative Western blot images of L-type Ca2+ channel and β-actin in cells with different treatments.
    Passage 19 21, supplied by ATCC, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    ALP attenuated oAβ-induced calcium influx. (a) bEND3 cells were incubated with the calcium indicator (2 μM Fluo-4, AM), pretreated with or without 20 nM ALP for 4 h, and then incubated with 5 μM oAβ or 1 μM A-23187 (a positive control) for 15 min. Normalized data are expressed as mean ± SE (***p < 0.001, comparing with control group; ○○○p < 0.001, comparing with 5 μM oAβ treatment only group) from four independent experiments (N = 4). (b) Representative Western blot images of L-type Ca2+ channel and β-actin in cells with different treatments.

    Journal: ACS chemical neuroscience

    Article Title: Azelnidipine Attenuates the Oxidative and NF κ B Pathways in Amyloid- β -Stimulated Cerebral Endothelial Cells

    doi: 10.1021/acschemneuro.8b00368

    Figure Lengend Snippet: ALP attenuated oAβ-induced calcium influx. (a) bEND3 cells were incubated with the calcium indicator (2 μM Fluo-4, AM), pretreated with or without 20 nM ALP for 4 h, and then incubated with 5 μM oAβ or 1 μM A-23187 (a positive control) for 15 min. Normalized data are expressed as mean ± SE (***p < 0.001, comparing with control group; ○○○p < 0.001, comparing with 5 μM oAβ treatment only group) from four independent experiments (N = 4). (b) Representative Western blot images of L-type Ca2+ channel and β-actin in cells with different treatments.

    Article Snippet: Passage 21 (P.21) bEND3 mouse cerebral endothelial cell line was purchased from ATCC (Manassas, VA).

    Techniques: Incubation, Positive Control, Western Blot

    ALP attenuated oAβ-induced phosphorylation of ERK p42 and p44. bEND3 cells were treated with 20 nM ALP for 4 h, and followed by treatment with or without 5 μM oAβ for 15 min. (a–c) Phospho- and total ERK p42/p44 and (d, e) phospho- and total p38 were quantified with Western blot analysis and expressed as ratio of phospho to total and as fraction percentages of the control group with the mean ± SD from four independent experiments (N = 4) (***p < 0.001, **p < 0.01, *p < 0.05 comparing with control group; ○○p < 0.01, ○p < 0.05 comparing with 5 μM oAβ treatment only group). (f, g) Representative Western blot images of total ERK p44/p42, p38, and β-actin.

    Journal: ACS chemical neuroscience

    Article Title: Azelnidipine Attenuates the Oxidative and NF κ B Pathways in Amyloid- β -Stimulated Cerebral Endothelial Cells

    doi: 10.1021/acschemneuro.8b00368

    Figure Lengend Snippet: ALP attenuated oAβ-induced phosphorylation of ERK p42 and p44. bEND3 cells were treated with 20 nM ALP for 4 h, and followed by treatment with or without 5 μM oAβ for 15 min. (a–c) Phospho- and total ERK p42/p44 and (d, e) phospho- and total p38 were quantified with Western blot analysis and expressed as ratio of phospho to total and as fraction percentages of the control group with the mean ± SD from four independent experiments (N = 4) (***p < 0.001, **p < 0.01, *p < 0.05 comparing with control group; ○○p < 0.01, ○p < 0.05 comparing with 5 μM oAβ treatment only group). (f, g) Representative Western blot images of total ERK p44/p42, p38, and β-actin.

    Article Snippet: Passage 21 (P.21) bEND3 mouse cerebral endothelial cell line was purchased from ATCC (Manassas, VA).

    Techniques: Western Blot

    Azelnidipine attenuated oAβ-induced phosphorylation of cPLA2. bEND3 cells were treated with 20 nM ALP for 4 h, followed by treatment with or without 5 μM oAβ for 30 min. (a, b) Phospho- and total cPLA2 were quantified by Western blot analysis. Data are expressed as a ratio of phospho- to total protein and normalized by the control group with the mean ± SD from three independent experiments (N = 3) (***p < 0.001, comparing with control group; ○○○p < 0.001, comparing with 5 μM oAβ treatment only group). (c) Representative Western blot images of total cPLA2 and β-actin.

    Journal: ACS chemical neuroscience

    Article Title: Azelnidipine Attenuates the Oxidative and NF κ B Pathways in Amyloid- β -Stimulated Cerebral Endothelial Cells

    doi: 10.1021/acschemneuro.8b00368

    Figure Lengend Snippet: Azelnidipine attenuated oAβ-induced phosphorylation of cPLA2. bEND3 cells were treated with 20 nM ALP for 4 h, followed by treatment with or without 5 μM oAβ for 30 min. (a, b) Phospho- and total cPLA2 were quantified by Western blot analysis. Data are expressed as a ratio of phospho- to total protein and normalized by the control group with the mean ± SD from three independent experiments (N = 3) (***p < 0.001, comparing with control group; ○○○p < 0.001, comparing with 5 μM oAβ treatment only group). (c) Representative Western blot images of total cPLA2 and β-actin.

    Article Snippet: Passage 21 (P.21) bEND3 mouse cerebral endothelial cell line was purchased from ATCC (Manassas, VA).

    Techniques: Western Blot

    Azelnidipine attenuated oAβ-induced superoxide anion production. bEND3 cells were treated with 20 nM ALP for 4 h, followed by treatment with or without 5 μM oAβ for 30 min. Superoxide anion production was quantified by measuring the DHE intensity within each sample. Data are normalized by the control group with the mean ± SD from three independent experiments (N = 3) (***p < 0.001, comparing with control group; ○○p < 0.01 comparing with 5 μM oAβ treatment only group).

    Journal: ACS chemical neuroscience

    Article Title: Azelnidipine Attenuates the Oxidative and NF κ B Pathways in Amyloid- β -Stimulated Cerebral Endothelial Cells

    doi: 10.1021/acschemneuro.8b00368

    Figure Lengend Snippet: Azelnidipine attenuated oAβ-induced superoxide anion production. bEND3 cells were treated with 20 nM ALP for 4 h, followed by treatment with or without 5 μM oAβ for 30 min. Superoxide anion production was quantified by measuring the DHE intensity within each sample. Data are normalized by the control group with the mean ± SD from three independent experiments (N = 3) (***p < 0.001, comparing with control group; ○○p < 0.01 comparing with 5 μM oAβ treatment only group).

    Article Snippet: Passage 21 (P.21) bEND3 mouse cerebral endothelial cell line was purchased from ATCC (Manassas, VA).

    Techniques:

    Azelnidipine attenuated oAβ-induced NFκB activation. bEND3 cells were treated with 20 nM ALP, 5 μM Aβ, both ALP and Aβ, 10 μM MAFP, both MAFP and Aβ, 2 μM BEL, and both BEL and Aβ or 100 ng/mL TNFα (positive control) to yield a total of nine datasets. (a) Nucleus staining is represented in red, and NFκB p65 subunit in green immunofluorescence. The merged images were obtained by superposing the nucleus staining and NFκB p65 subunit in the same field acquired using different filter sets. (b) NFκB activation was quantified by the ratio of NFκB p65 subunit intensity in nuclei to that in cytoplasm. Data are expressed with the mean ± SD from four independent experiments reported (N = 4) (*p < 0.05, **p < 0.01, comparing with control group; ○p < 0.05, comparing with 5 μM oAβ treatment only group).

    Journal: ACS chemical neuroscience

    Article Title: Azelnidipine Attenuates the Oxidative and NF κ B Pathways in Amyloid- β -Stimulated Cerebral Endothelial Cells

    doi: 10.1021/acschemneuro.8b00368

    Figure Lengend Snippet: Azelnidipine attenuated oAβ-induced NFκB activation. bEND3 cells were treated with 20 nM ALP, 5 μM Aβ, both ALP and Aβ, 10 μM MAFP, both MAFP and Aβ, 2 μM BEL, and both BEL and Aβ or 100 ng/mL TNFα (positive control) to yield a total of nine datasets. (a) Nucleus staining is represented in red, and NFκB p65 subunit in green immunofluorescence. The merged images were obtained by superposing the nucleus staining and NFκB p65 subunit in the same field acquired using different filter sets. (b) NFκB activation was quantified by the ratio of NFκB p65 subunit intensity in nuclei to that in cytoplasm. Data are expressed with the mean ± SD from four independent experiments reported (N = 4) (*p < 0.05, **p < 0.01, comparing with control group; ○p < 0.05, comparing with 5 μM oAβ treatment only group).

    Article Snippet: Passage 21 (P.21) bEND3 mouse cerebral endothelial cell line was purchased from ATCC (Manassas, VA).

    Techniques: Activation Assay, Positive Control, Staining, Immunofluorescence