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platelet activation marker p selectin  (Bioss)


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    Structured Review

    Bioss platelet activation marker p selectin
    Cigarette smoke (CS)‐induced vascular oxidative stress and platelet aggregation were prevented by apocynin treatment. Mice were exposed to CS or room air (sham) for 8 weeks with i.p. injection of apocynin (5 mg·kg −1 ·day −1 ) or vehicle (saline). Representative immunofluorescence images of thoracic aorta section stained with 3‐nitrotyrosine (3‐NT; a), platelet surface marker (CD41; b), or platelet activation marker <t>(CD62p;</t> c), with positive staining in green and nuclei in blue (DAPI). White arrows indicate positive stains and the respective positive stains were quantified as described in methods. Data are expressed as mean + SEM (n = 8 mice per group) and analysed by two‐way ANOVA with multiple comparisons and Tukey post hoc test. * P < 0.05 denotes differences between the compared groups.
    Platelet Activation Marker P Selectin, supplied by Bioss, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/platelet+activation+marker+p+selectin/pmc10953324-81-51-59
    Average 86 stars, based on 1 article reviews
    platelet activation marker p selectin - by Bioz Stars, 2026-09
    86/100 stars

    Images

    1) Product Images from "Inhibition of oxidative stress by apocynin attenuated chronic obstructive pulmonary disease progression and vascular injury by cigarette smoke exposure"

    Article Title: Inhibition of oxidative stress by apocynin attenuated chronic obstructive pulmonary disease progression and vascular injury by cigarette smoke exposure

    Journal: British Journal of Pharmacology

    doi: 10.1111/bph.16068

    Cigarette smoke (CS)‐induced vascular oxidative stress and platelet aggregation were prevented by apocynin treatment. Mice were exposed to CS or room air (sham) for 8 weeks with i.p. injection of apocynin (5 mg·kg −1 ·day −1 ) or vehicle (saline). Representative immunofluorescence images of thoracic aorta section stained with 3‐nitrotyrosine (3‐NT; a), platelet surface marker (CD41; b), or platelet activation marker (CD62p; c), with positive staining in green and nuclei in blue (DAPI). White arrows indicate positive stains and the respective positive stains were quantified as described in methods. Data are expressed as mean + SEM (n = 8 mice per group) and analysed by two‐way ANOVA with multiple comparisons and Tukey post hoc test. * P < 0.05 denotes differences between the compared groups.
    Figure Legend Snippet: Cigarette smoke (CS)‐induced vascular oxidative stress and platelet aggregation were prevented by apocynin treatment. Mice were exposed to CS or room air (sham) for 8 weeks with i.p. injection of apocynin (5 mg·kg −1 ·day −1 ) or vehicle (saline). Representative immunofluorescence images of thoracic aorta section stained with 3‐nitrotyrosine (3‐NT; a), platelet surface marker (CD41; b), or platelet activation marker (CD62p; c), with positive staining in green and nuclei in blue (DAPI). White arrows indicate positive stains and the respective positive stains were quantified as described in methods. Data are expressed as mean + SEM (n = 8 mice per group) and analysed by two‐way ANOVA with multiple comparisons and Tukey post hoc test. * P < 0.05 denotes differences between the compared groups.

    Techniques Used: Injection, Saline, Immunofluorescence, Staining, Marker, Activation Assay

    Long term cigarette smoke (CS)‐induced loss of eNOS, vascular oxidative stress and platelet activation were attenuated by apocynin treatment. Mice were exposed to CS or room air (sham) for 8 weeks with i.p. injection of apocynin (5 mg·kg −1 ·day −1 ) or vehicle (saline). Representative immunofluorescence images of thoracic aorta section stained with eNOS (a), 3‐NT (b), platelet surface CD41 (c), or platelet activation CD62p (d), with positive staining in green and nuclei in blue (DAPI). White arrows indicate positive stains and the respective positive stains were quantified as described in methods. Data are expressed as mean + SEM (n = 8 mice per group) and analysed by two‐way ANOVA with multiple comparisons and Tukey post hoc test. * P < 0.05, denotes differences between the compared groups.
    Figure Legend Snippet: Long term cigarette smoke (CS)‐induced loss of eNOS, vascular oxidative stress and platelet activation were attenuated by apocynin treatment. Mice were exposed to CS or room air (sham) for 8 weeks with i.p. injection of apocynin (5 mg·kg −1 ·day −1 ) or vehicle (saline). Representative immunofluorescence images of thoracic aorta section stained with eNOS (a), 3‐NT (b), platelet surface CD41 (c), or platelet activation CD62p (d), with positive staining in green and nuclei in blue (DAPI). White arrows indicate positive stains and the respective positive stains were quantified as described in methods. Data are expressed as mean + SEM (n = 8 mice per group) and analysed by two‐way ANOVA with multiple comparisons and Tukey post hoc test. * P < 0.05, denotes differences between the compared groups.

    Techniques Used: Activation Assay, Injection, Saline, Immunofluorescence, Staining

    Related Articles

    Immunostaining:

    Article Title: Inhibition of oxidative stress by apocynin attenuated chronic obstructive pulmonary disease progression and vascular injury by cigarette smoke exposure
    Article Snippet: .. For aortic immunostaining, specific primary antibodies were used to detect vascular endothelial nitric oxide synthase (eNOS ; anti‐NOS3 at 1:100 dilution; Thermo Fisher Scientific, USA), vascular peroxynitrite (anti‐3‐Nitrotyrosine [3‐NT] at 1:100 dilution; Thermofisher Scientific, NY, USA), platelet surface marker Integrin alpha 2b (anti‐CD41 at 1:100 dilution; Bioss Antibodies, MA, USA) and platelet activation marker p‐selectin (anti‐CD62p at 1:100 dilution; Bioss Antibodies, MA, USA). .. After an overnight incubation at 4°C, the sections were washed before exposure to fluorescent‐conjugated secondary antibody (Goat anti‐Rabbit IgG FluorTM 488; Thermofisher Scientific, NY, USA) for 2 h at room temperature, light protected.

    Marker:

    Article Title: Inhibition of oxidative stress by apocynin attenuated chronic obstructive pulmonary disease progression and vascular injury by cigarette smoke exposure
    Article Snippet: .. For aortic immunostaining, specific primary antibodies were used to detect vascular endothelial nitric oxide synthase (eNOS ; anti‐NOS3 at 1:100 dilution; Thermo Fisher Scientific, USA), vascular peroxynitrite (anti‐3‐Nitrotyrosine [3‐NT] at 1:100 dilution; Thermofisher Scientific, NY, USA), platelet surface marker Integrin alpha 2b (anti‐CD41 at 1:100 dilution; Bioss Antibodies, MA, USA) and platelet activation marker p‐selectin (anti‐CD62p at 1:100 dilution; Bioss Antibodies, MA, USA). .. After an overnight incubation at 4°C, the sections were washed before exposure to fluorescent‐conjugated secondary antibody (Goat anti‐Rabbit IgG FluorTM 488; Thermofisher Scientific, NY, USA) for 2 h at room temperature, light protected.

    Activation Assay:

    Article Title: Inhibition of oxidative stress by apocynin attenuated chronic obstructive pulmonary disease progression and vascular injury by cigarette smoke exposure
    Article Snippet: .. For aortic immunostaining, specific primary antibodies were used to detect vascular endothelial nitric oxide synthase (eNOS ; anti‐NOS3 at 1:100 dilution; Thermo Fisher Scientific, USA), vascular peroxynitrite (anti‐3‐Nitrotyrosine [3‐NT] at 1:100 dilution; Thermofisher Scientific, NY, USA), platelet surface marker Integrin alpha 2b (anti‐CD41 at 1:100 dilution; Bioss Antibodies, MA, USA) and platelet activation marker p‐selectin (anti‐CD62p at 1:100 dilution; Bioss Antibodies, MA, USA). .. After an overnight incubation at 4°C, the sections were washed before exposure to fluorescent‐conjugated secondary antibody (Goat anti‐Rabbit IgG FluorTM 488; Thermofisher Scientific, NY, USA) for 2 h at room temperature, light protected.



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    Cigarette smoke (CS)‐induced vascular oxidative stress and platelet aggregation were prevented by apocynin treatment. Mice were exposed to CS or room air (sham) for 8 weeks with i.p. injection of apocynin (5 mg·kg −1 ·day −1 ) or vehicle (saline). Representative immunofluorescence images of thoracic aorta section stained with 3‐nitrotyrosine (3‐NT; a), platelet surface marker (CD41; b), or platelet activation marker <t>(CD62p;</t> c), with positive staining in green and nuclei in blue (DAPI). White arrows indicate positive stains and the respective positive stains were quantified as described in methods. Data are expressed as mean + SEM (n = 8 mice per group) and analysed by two‐way ANOVA with multiple comparisons and Tukey post hoc test. * P < 0.05 denotes differences between the compared groups.
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    Image Search Results


    Cigarette smoke (CS)‐induced vascular oxidative stress and platelet aggregation were prevented by apocynin treatment. Mice were exposed to CS or room air (sham) for 8 weeks with i.p. injection of apocynin (5 mg·kg −1 ·day −1 ) or vehicle (saline). Representative immunofluorescence images of thoracic aorta section stained with 3‐nitrotyrosine (3‐NT; a), platelet surface marker (CD41; b), or platelet activation marker (CD62p; c), with positive staining in green and nuclei in blue (DAPI). White arrows indicate positive stains and the respective positive stains were quantified as described in methods. Data are expressed as mean + SEM (n = 8 mice per group) and analysed by two‐way ANOVA with multiple comparisons and Tukey post hoc test. * P < 0.05 denotes differences between the compared groups.

    Journal: British Journal of Pharmacology

    Article Title: Inhibition of oxidative stress by apocynin attenuated chronic obstructive pulmonary disease progression and vascular injury by cigarette smoke exposure

    doi: 10.1111/bph.16068

    Figure Lengend Snippet: Cigarette smoke (CS)‐induced vascular oxidative stress and platelet aggregation were prevented by apocynin treatment. Mice were exposed to CS or room air (sham) for 8 weeks with i.p. injection of apocynin (5 mg·kg −1 ·day −1 ) or vehicle (saline). Representative immunofluorescence images of thoracic aorta section stained with 3‐nitrotyrosine (3‐NT; a), platelet surface marker (CD41; b), or platelet activation marker (CD62p; c), with positive staining in green and nuclei in blue (DAPI). White arrows indicate positive stains and the respective positive stains were quantified as described in methods. Data are expressed as mean + SEM (n = 8 mice per group) and analysed by two‐way ANOVA with multiple comparisons and Tukey post hoc test. * P < 0.05 denotes differences between the compared groups.

    Article Snippet: For aortic immunostaining, specific primary antibodies were used to detect vascular endothelial nitric oxide synthase (eNOS ; anti‐NOS3 at 1:100 dilution; Thermo Fisher Scientific, USA), vascular peroxynitrite (anti‐3‐Nitrotyrosine [3‐NT] at 1:100 dilution; Thermofisher Scientific, NY, USA), platelet surface marker Integrin alpha 2b (anti‐CD41 at 1:100 dilution; Bioss Antibodies, MA, USA) and platelet activation marker p‐selectin (anti‐CD62p at 1:100 dilution; Bioss Antibodies, MA, USA).

    Techniques: Injection, Saline, Immunofluorescence, Staining, Marker, Activation Assay

    Long term cigarette smoke (CS)‐induced loss of eNOS, vascular oxidative stress and platelet activation were attenuated by apocynin treatment. Mice were exposed to CS or room air (sham) for 8 weeks with i.p. injection of apocynin (5 mg·kg −1 ·day −1 ) or vehicle (saline). Representative immunofluorescence images of thoracic aorta section stained with eNOS (a), 3‐NT (b), platelet surface CD41 (c), or platelet activation CD62p (d), with positive staining in green and nuclei in blue (DAPI). White arrows indicate positive stains and the respective positive stains were quantified as described in methods. Data are expressed as mean + SEM (n = 8 mice per group) and analysed by two‐way ANOVA with multiple comparisons and Tukey post hoc test. * P < 0.05, denotes differences between the compared groups.

    Journal: British Journal of Pharmacology

    Article Title: Inhibition of oxidative stress by apocynin attenuated chronic obstructive pulmonary disease progression and vascular injury by cigarette smoke exposure

    doi: 10.1111/bph.16068

    Figure Lengend Snippet: Long term cigarette smoke (CS)‐induced loss of eNOS, vascular oxidative stress and platelet activation were attenuated by apocynin treatment. Mice were exposed to CS or room air (sham) for 8 weeks with i.p. injection of apocynin (5 mg·kg −1 ·day −1 ) or vehicle (saline). Representative immunofluorescence images of thoracic aorta section stained with eNOS (a), 3‐NT (b), platelet surface CD41 (c), or platelet activation CD62p (d), with positive staining in green and nuclei in blue (DAPI). White arrows indicate positive stains and the respective positive stains were quantified as described in methods. Data are expressed as mean + SEM (n = 8 mice per group) and analysed by two‐way ANOVA with multiple comparisons and Tukey post hoc test. * P < 0.05, denotes differences between the compared groups.

    Article Snippet: For aortic immunostaining, specific primary antibodies were used to detect vascular endothelial nitric oxide synthase (eNOS ; anti‐NOS3 at 1:100 dilution; Thermo Fisher Scientific, USA), vascular peroxynitrite (anti‐3‐Nitrotyrosine [3‐NT] at 1:100 dilution; Thermofisher Scientific, NY, USA), platelet surface marker Integrin alpha 2b (anti‐CD41 at 1:100 dilution; Bioss Antibodies, MA, USA) and platelet activation marker p‐selectin (anti‐CD62p at 1:100 dilution; Bioss Antibodies, MA, USA).

    Techniques: Activation Assay, Injection, Saline, Immunofluorescence, Staining