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ER reporter assay with N2A and N2Aswe (A) and ER stable transfected SK-N-MC cells (B). Activation of the ER response element was plotted as fold induction of luciferase activity normalized to untreated cells (n.t.). Treatment: n.t., untreated; ICI, <t>ICI</t> <t>182780</t> at final concentration (f.c) of 10−6 M; E-7, E2 f.c. 10−7 M; E-8, oestrogen f.c. 10−8 M, N-6, nebivolol f.c. 10−6 M. The results shown represent more than three independent studies. Significance is defined as follows: *P < 0.05; ***P < 0.001 compared with untreated cells (anova).
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ER reporter assay with N2A and N2Aswe (A) and ER stable transfected SK-N-MC cells (B). Activation of the ER response element was plotted as fold induction of luciferase activity normalized to untreated cells (n.t.). Treatment: n.t., untreated; ICI, <t>ICI</t> <t>182780</t> at final concentration (f.c) of 10−6 M; E-7, E2 f.c. 10−7 M; E-8, oestrogen f.c. 10−8 M, N-6, nebivolol f.c. 10−6 M. The results shown represent more than three independent studies. Significance is defined as follows: *P < 0.05; ***P < 0.001 compared with untreated cells (anova).
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ER reporter assay with N2A and N2Aswe (A) and ER stable transfected SK-N-MC cells (B). Activation of the ER response element was plotted as fold induction of luciferase activity normalized to untreated cells (n.t.). Treatment: n.t., untreated; ICI, <t>ICI</t> <t>182780</t> at final concentration (f.c) of 10−6 M; E-7, E2 f.c. 10−7 M; E-8, oestrogen f.c. 10−8 M, N-6, nebivolol f.c. 10−6 M. The results shown represent more than three independent studies. Significance is defined as follows: *P < 0.05; ***P < 0.001 compared with untreated cells (anova).
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ER reporter assay with N2A and N2Aswe (A) and ER stable transfected SK-N-MC cells (B). Activation of the ER response element was plotted as fold induction of luciferase activity normalized to untreated cells (n.t.). Treatment: n.t., untreated; ICI, ICI 182780 at final concentration (f.c) of 10−6 M; E-7, E2 f.c. 10−7 M; E-8, oestrogen f.c. 10−8 M, N-6, nebivolol f.c. 10−6 M. The results shown represent more than three independent studies. Significance is defined as follows: *P < 0.05; ***P < 0.001 compared with untreated cells (anova).

Journal: British Journal of Pharmacology

Article Title: The selective ? 1 -adrenoceptor antagonist nebivolol is a potential oestrogen receptor agonist with neuroprotective abilities

doi: 10.1111/j.1476-5381.2009.00610.x

Figure Lengend Snippet: ER reporter assay with N2A and N2Aswe (A) and ER stable transfected SK-N-MC cells (B). Activation of the ER response element was plotted as fold induction of luciferase activity normalized to untreated cells (n.t.). Treatment: n.t., untreated; ICI, ICI 182780 at final concentration (f.c) of 10−6 M; E-7, E2 f.c. 10−7 M; E-8, oestrogen f.c. 10−8 M, N-6, nebivolol f.c. 10−6 M. The results shown represent more than three independent studies. Significance is defined as follows: *P < 0.05; ***P < 0.001 compared with untreated cells (anova).

Article Snippet: 17-β Oestradiol (E2) was purchased from Sigma Chemical Co., the ER antagonist ICI 182780 was from Tocris/Biotrend (Cologne, Germany), non-selective NOS inhibitor l -NMMA was purchased from Calbiochem/Merck (Darmstadt, Germany) and d -/ l -nebivolol was provided by Berlin Chemie/Menarini AG (Berlin, Germany).

Techniques: Reporter Assay, Transfection, Activation Assay, Luciferase, Activity Assay, Concentration Assay

Nebivolol and E2 increased the survival of N2Aswe cells after H2O2 or PQ-induced oxidative stress. Cells were pretreated with oestrogen (f.c. 10−8 M), different nebivolol concentrations as indicated, ICI 182780 (ICI, f.c. 10−6 M), l-NMMA (f.c. 10−6 M) and oestrogen and nebivolol together with ICI 182780 and l-NMMA, followed by exposure to H2O2 (A) and PQ (0–1000 µM) (B). Data show mean cell survival from a representative experiment (n = 9). *P < 0.05, compared with untreated cells (n.t) (anova).

Journal: British Journal of Pharmacology

Article Title: The selective ? 1 -adrenoceptor antagonist nebivolol is a potential oestrogen receptor agonist with neuroprotective abilities

doi: 10.1111/j.1476-5381.2009.00610.x

Figure Lengend Snippet: Nebivolol and E2 increased the survival of N2Aswe cells after H2O2 or PQ-induced oxidative stress. Cells were pretreated with oestrogen (f.c. 10−8 M), different nebivolol concentrations as indicated, ICI 182780 (ICI, f.c. 10−6 M), l-NMMA (f.c. 10−6 M) and oestrogen and nebivolol together with ICI 182780 and l-NMMA, followed by exposure to H2O2 (A) and PQ (0–1000 µM) (B). Data show mean cell survival from a representative experiment (n = 9). *P < 0.05, compared with untreated cells (n.t) (anova).

Article Snippet: 17-β Oestradiol (E2) was purchased from Sigma Chemical Co., the ER antagonist ICI 182780 was from Tocris/Biotrend (Cologne, Germany), non-selective NOS inhibitor l -NMMA was purchased from Calbiochem/Merck (Darmstadt, Germany) and d -/ l -nebivolol was provided by Berlin Chemie/Menarini AG (Berlin, Germany).

Techniques:

Relative mRNA expression ratios of E2 and nebivolol-regulated genes in N2Aswe and SK-N-MC ERα and ERβ over-expressing cells. Cells were treated with E2 (f.c. 10−8 M), nebivolol (10−6 M and 10−8M) and oestrogen and nebivolol (10−8M) together with ICI 182780 for 18 h. Genes were considered differentially expressed when the expression levels between untreated and treated cells (expressed as a ratio) were more than 1.5-fold difference (dotted lines) and a P value <0.05. Fold change of gene expression levels was based on the ΔΔCt method with normalization of the raw data to housekeeping genes by using the relative expression software tool (REST-MCS V2.0).

Journal: British Journal of Pharmacology

Article Title: The selective ? 1 -adrenoceptor antagonist nebivolol is a potential oestrogen receptor agonist with neuroprotective abilities

doi: 10.1111/j.1476-5381.2009.00610.x

Figure Lengend Snippet: Relative mRNA expression ratios of E2 and nebivolol-regulated genes in N2Aswe and SK-N-MC ERα and ERβ over-expressing cells. Cells were treated with E2 (f.c. 10−8 M), nebivolol (10−6 M and 10−8M) and oestrogen and nebivolol (10−8M) together with ICI 182780 for 18 h. Genes were considered differentially expressed when the expression levels between untreated and treated cells (expressed as a ratio) were more than 1.5-fold difference (dotted lines) and a P value <0.05. Fold change of gene expression levels was based on the ΔΔCt method with normalization of the raw data to housekeeping genes by using the relative expression software tool (REST-MCS V2.0).

Article Snippet: 17-β Oestradiol (E2) was purchased from Sigma Chemical Co., the ER antagonist ICI 182780 was from Tocris/Biotrend (Cologne, Germany), non-selective NOS inhibitor l -NMMA was purchased from Calbiochem/Merck (Darmstadt, Germany) and d -/ l -nebivolol was provided by Berlin Chemie/Menarini AG (Berlin, Germany).

Techniques: Expressing, Software

Modulation of the generation of sAPPα and Aβswe induced by the enhanced α-secretase activity observed after nebivolol and E2 treatment. (A) Quantification of sAPPα (elisa). (B) Quantification of Aβ swe (elisa). (C) α-Secretase activity assay; activity was plotted as fold induction normalized to untreated cells (n.t.). Treatments: n.t., untreated; ICI, ICI 182780 at final concentration (f.c) of 10−6 M; E-7, oestrogen f.c. 10−7 M; E-8, oestrogen f.c. 10−8 M, N-6, nebivolol f.c. 10−6 M, N-7, nebivolol f.c. 10−7 M, N-8, nebivolol f.c. 10−8 M. The histograms represent results from more than three independent studies. **P < 0.005, compared with untreated cells of the same kind (anova).

Journal: British Journal of Pharmacology

Article Title: The selective ? 1 -adrenoceptor antagonist nebivolol is a potential oestrogen receptor agonist with neuroprotective abilities

doi: 10.1111/j.1476-5381.2009.00610.x

Figure Lengend Snippet: Modulation of the generation of sAPPα and Aβswe induced by the enhanced α-secretase activity observed after nebivolol and E2 treatment. (A) Quantification of sAPPα (elisa). (B) Quantification of Aβ swe (elisa). (C) α-Secretase activity assay; activity was plotted as fold induction normalized to untreated cells (n.t.). Treatments: n.t., untreated; ICI, ICI 182780 at final concentration (f.c) of 10−6 M; E-7, oestrogen f.c. 10−7 M; E-8, oestrogen f.c. 10−8 M, N-6, nebivolol f.c. 10−6 M, N-7, nebivolol f.c. 10−7 M, N-8, nebivolol f.c. 10−8 M. The histograms represent results from more than three independent studies. **P < 0.005, compared with untreated cells of the same kind (anova).

Article Snippet: 17-β Oestradiol (E2) was purchased from Sigma Chemical Co., the ER antagonist ICI 182780 was from Tocris/Biotrend (Cologne, Germany), non-selective NOS inhibitor l -NMMA was purchased from Calbiochem/Merck (Darmstadt, Germany) and d -/ l -nebivolol was provided by Berlin Chemie/Menarini AG (Berlin, Germany).

Techniques: Activity Assay, Enzyme-linked Immunosorbent Assay, Concentration Assay