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  • 94
    Alomone Labs alpha bungarotoxin
    Cholinergic stimulation attenuates LPS-induced IL-8 response in SW480 cells via <t>a7nAChR.</t> Expression of ACHRs in SW480 cells (A) . SW480 cells (5 x 10 4 /200µl) were stimulated with LPS (100ng/ml) in the presence of different agonist and antagonists. IL-8 was measured in cell-free supernatants 20h after LPS stimulation. Cells were stimulated with LPS 20min prior to acetylcholine (ACh, 10µM), nicotine (10µM), and muscarine (10µM) stimulation (B) . Cells were pretreated (20min) with the non-selective nAChR antagonist Mecamylamine (Mec, <t>100µM)</t> followed by treatment with ACh (10µM), 20min prior to LPS stimulation (C) . Cells were pretreated (20min) with the selective a7nAChR antagonist <t>alpha-Bungarotoxin</t> (a-BTX, 100µM) followed by treatment with GTS-21 (100µM), 20min prior to LPS stimulation (D) . Cells were pretreated (20min) with GTS-21 (100µM) followed by stimulation with LPS. Phospho (p)-NFĸB-p65 was measured 4h after LPS stimulation (E) . Cells were pretreated (20min) with DMSO (0.01%, control) or tyrphostin AG490 (1µM) or wortmannin (1µM) followed by stimulation with LPS (100ng/ml), 20min prior to treatment with a7nAChR agonist GTS-21 (20min) (F) . Cell viability was assessed by colorimetric MTS assay (G) . Each point in the scatter plots with bar represent triplicates or quadruplicates ± SEM. Data are representative of three independent experiments. Significance was determined using one-way ANOVA multiple comparison analysis (A–D) and paired t test (E, F) with *p ≤ 0.05; **p ≤ 0.01; ***p ≤ 0.005. ns, not significant. n.d., not detectable.
    Alpha Bungarotoxin, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    86
    Vitex Inc b 100
    Cholinergic stimulation attenuates LPS-induced IL-8 response in SW480 cells via <t>a7nAChR.</t> Expression of ACHRs in SW480 cells (A) . SW480 cells (5 x 10 4 /200µl) were stimulated with LPS (100ng/ml) in the presence of different agonist and antagonists. IL-8 was measured in cell-free supernatants 20h after LPS stimulation. Cells were stimulated with LPS 20min prior to acetylcholine (ACh, 10µM), nicotine (10µM), and muscarine (10µM) stimulation (B) . Cells were pretreated (20min) with the non-selective nAChR antagonist Mecamylamine (Mec, <t>100µM)</t> followed by treatment with ACh (10µM), 20min prior to LPS stimulation (C) . Cells were pretreated (20min) with the selective a7nAChR antagonist <t>alpha-Bungarotoxin</t> (a-BTX, 100µM) followed by treatment with GTS-21 (100µM), 20min prior to LPS stimulation (D) . Cells were pretreated (20min) with GTS-21 (100µM) followed by stimulation with LPS. Phospho (p)-NFĸB-p65 was measured 4h after LPS stimulation (E) . Cells were pretreated (20min) with DMSO (0.01%, control) or tyrphostin AG490 (1µM) or wortmannin (1µM) followed by stimulation with LPS (100ng/ml), 20min prior to treatment with a7nAChR agonist GTS-21 (20min) (F) . Cell viability was assessed by colorimetric MTS assay (G) . Each point in the scatter plots with bar represent triplicates or quadruplicates ± SEM. Data are representative of three independent experiments. Significance was determined using one-way ANOVA multiple comparison analysis (A–D) and paired t test (E, F) with *p ≤ 0.05; **p ≤ 0.01; ***p ≤ 0.005. ns, not significant. n.d., not detectable.
    B 100, supplied by Vitex Inc, 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/result/b 100/product/Vitex Inc
    Average 86 stars, based on 1 article reviews
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    b 100 - by Bioz Stars, 2023-02
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    86
    BUCHI AG b 100
    Cholinergic stimulation attenuates LPS-induced IL-8 response in SW480 cells via <t>a7nAChR.</t> Expression of ACHRs in SW480 cells (A) . SW480 cells (5 x 10 4 /200µl) were stimulated with LPS (100ng/ml) in the presence of different agonist and antagonists. IL-8 was measured in cell-free supernatants 20h after LPS stimulation. Cells were stimulated with LPS 20min prior to acetylcholine (ACh, 10µM), nicotine (10µM), and muscarine (10µM) stimulation (B) . Cells were pretreated (20min) with the non-selective nAChR antagonist Mecamylamine (Mec, <t>100µM)</t> followed by treatment with ACh (10µM), 20min prior to LPS stimulation (C) . Cells were pretreated (20min) with the selective a7nAChR antagonist <t>alpha-Bungarotoxin</t> (a-BTX, 100µM) followed by treatment with GTS-21 (100µM), 20min prior to LPS stimulation (D) . Cells were pretreated (20min) with GTS-21 (100µM) followed by stimulation with LPS. Phospho (p)-NFĸB-p65 was measured 4h after LPS stimulation (E) . Cells were pretreated (20min) with DMSO (0.01%, control) or tyrphostin AG490 (1µM) or wortmannin (1µM) followed by stimulation with LPS (100ng/ml), 20min prior to treatment with a7nAChR agonist GTS-21 (20min) (F) . Cell viability was assessed by colorimetric MTS assay (G) . Each point in the scatter plots with bar represent triplicates or quadruplicates ± SEM. Data are representative of three independent experiments. Significance was determined using one-way ANOVA multiple comparison analysis (A–D) and paired t test (E, F) with *p ≤ 0.05; **p ≤ 0.01; ***p ≤ 0.005. ns, not significant. n.d., not detectable.
    B 100, supplied by BUCHI AG, 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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    94
    Excel Scientific gas permeable membranes
    Cholinergic stimulation attenuates LPS-induced IL-8 response in SW480 cells via <t>a7nAChR.</t> Expression of ACHRs in SW480 cells (A) . SW480 cells (5 x 10 4 /200µl) were stimulated with LPS (100ng/ml) in the presence of different agonist and antagonists. IL-8 was measured in cell-free supernatants 20h after LPS stimulation. Cells were stimulated with LPS 20min prior to acetylcholine (ACh, 10µM), nicotine (10µM), and muscarine (10µM) stimulation (B) . Cells were pretreated (20min) with the non-selective nAChR antagonist Mecamylamine (Mec, <t>100µM)</t> followed by treatment with ACh (10µM), 20min prior to LPS stimulation (C) . Cells were pretreated (20min) with the selective a7nAChR antagonist <t>alpha-Bungarotoxin</t> (a-BTX, 100µM) followed by treatment with GTS-21 (100µM), 20min prior to LPS stimulation (D) . Cells were pretreated (20min) with GTS-21 (100µM) followed by stimulation with LPS. Phospho (p)-NFĸB-p65 was measured 4h after LPS stimulation (E) . Cells were pretreated (20min) with DMSO (0.01%, control) or tyrphostin AG490 (1µM) or wortmannin (1µM) followed by stimulation with LPS (100ng/ml), 20min prior to treatment with a7nAChR agonist GTS-21 (20min) (F) . Cell viability was assessed by colorimetric MTS assay (G) . Each point in the scatter plots with bar represent triplicates or quadruplicates ± SEM. Data are representative of three independent experiments. Significance was determined using one-way ANOVA multiple comparison analysis (A–D) and paired t test (E, F) with *p ≤ 0.05; **p ≤ 0.01; ***p ≤ 0.005. ns, not significant. n.d., not detectable.
    Gas Permeable Membranes, supplied by Excel Scientific, 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/gas permeable membranes/product/Excel Scientific
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    85
    VHG Labs biodiesel standard
    Cholinergic stimulation attenuates LPS-induced IL-8 response in SW480 cells via <t>a7nAChR.</t> Expression of ACHRs in SW480 cells (A) . SW480 cells (5 x 10 4 /200µl) were stimulated with LPS (100ng/ml) in the presence of different agonist and antagonists. IL-8 was measured in cell-free supernatants 20h after LPS stimulation. Cells were stimulated with LPS 20min prior to acetylcholine (ACh, 10µM), nicotine (10µM), and muscarine (10µM) stimulation (B) . Cells were pretreated (20min) with the non-selective nAChR antagonist Mecamylamine (Mec, <t>100µM)</t> followed by treatment with ACh (10µM), 20min prior to LPS stimulation (C) . Cells were pretreated (20min) with the selective a7nAChR antagonist <t>alpha-Bungarotoxin</t> (a-BTX, 100µM) followed by treatment with GTS-21 (100µM), 20min prior to LPS stimulation (D) . Cells were pretreated (20min) with GTS-21 (100µM) followed by stimulation with LPS. Phospho (p)-NFĸB-p65 was measured 4h after LPS stimulation (E) . Cells were pretreated (20min) with DMSO (0.01%, control) or tyrphostin AG490 (1µM) or wortmannin (1µM) followed by stimulation with LPS (100ng/ml), 20min prior to treatment with a7nAChR agonist GTS-21 (20min) (F) . Cell viability was assessed by colorimetric MTS assay (G) . Each point in the scatter plots with bar represent triplicates or quadruplicates ± SEM. Data are representative of three independent experiments. Significance was determined using one-way ANOVA multiple comparison analysis (A–D) and paired t test (E, F) with *p ≤ 0.05; **p ≤ 0.01; ***p ≤ 0.005. ns, not significant. n.d., not detectable.
    Biodiesel Standard, supplied by VHG Labs, used in various techniques. Bioz Stars score: 85/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/biodiesel standard/product/VHG Labs
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    Image Search Results


    Cholinergic stimulation attenuates LPS-induced IL-8 response in SW480 cells via a7nAChR. Expression of ACHRs in SW480 cells (A) . SW480 cells (5 x 10 4 /200µl) were stimulated with LPS (100ng/ml) in the presence of different agonist and antagonists. IL-8 was measured in cell-free supernatants 20h after LPS stimulation. Cells were stimulated with LPS 20min prior to acetylcholine (ACh, 10µM), nicotine (10µM), and muscarine (10µM) stimulation (B) . Cells were pretreated (20min) with the non-selective nAChR antagonist Mecamylamine (Mec, 100µM) followed by treatment with ACh (10µM), 20min prior to LPS stimulation (C) . Cells were pretreated (20min) with the selective a7nAChR antagonist alpha-Bungarotoxin (a-BTX, 100µM) followed by treatment with GTS-21 (100µM), 20min prior to LPS stimulation (D) . Cells were pretreated (20min) with GTS-21 (100µM) followed by stimulation with LPS. Phospho (p)-NFĸB-p65 was measured 4h after LPS stimulation (E) . Cells were pretreated (20min) with DMSO (0.01%, control) or tyrphostin AG490 (1µM) or wortmannin (1µM) followed by stimulation with LPS (100ng/ml), 20min prior to treatment with a7nAChR agonist GTS-21 (20min) (F) . Cell viability was assessed by colorimetric MTS assay (G) . Each point in the scatter plots with bar represent triplicates or quadruplicates ± SEM. Data are representative of three independent experiments. Significance was determined using one-way ANOVA multiple comparison analysis (A–D) and paired t test (E, F) with *p ≤ 0.05; **p ≤ 0.01; ***p ≤ 0.005. ns, not significant. n.d., not detectable.

    Journal: Frontiers in Immunology

    Article Title: Cholinergic Signaling Attenuates Pro-Inflammatory Interleukin-8 Response in Colonic Epithelial Cells

    doi: 10.3389/fimmu.2021.781147

    Figure Lengend Snippet: Cholinergic stimulation attenuates LPS-induced IL-8 response in SW480 cells via a7nAChR. Expression of ACHRs in SW480 cells (A) . SW480 cells (5 x 10 4 /200µl) were stimulated with LPS (100ng/ml) in the presence of different agonist and antagonists. IL-8 was measured in cell-free supernatants 20h after LPS stimulation. Cells were stimulated with LPS 20min prior to acetylcholine (ACh, 10µM), nicotine (10µM), and muscarine (10µM) stimulation (B) . Cells were pretreated (20min) with the non-selective nAChR antagonist Mecamylamine (Mec, 100µM) followed by treatment with ACh (10µM), 20min prior to LPS stimulation (C) . Cells were pretreated (20min) with the selective a7nAChR antagonist alpha-Bungarotoxin (a-BTX, 100µM) followed by treatment with GTS-21 (100µM), 20min prior to LPS stimulation (D) . Cells were pretreated (20min) with GTS-21 (100µM) followed by stimulation with LPS. Phospho (p)-NFĸB-p65 was measured 4h after LPS stimulation (E) . Cells were pretreated (20min) with DMSO (0.01%, control) or tyrphostin AG490 (1µM) or wortmannin (1µM) followed by stimulation with LPS (100ng/ml), 20min prior to treatment with a7nAChR agonist GTS-21 (20min) (F) . Cell viability was assessed by colorimetric MTS assay (G) . Each point in the scatter plots with bar represent triplicates or quadruplicates ± SEM. Data are representative of three independent experiments. Significance was determined using one-way ANOVA multiple comparison analysis (A–D) and paired t test (E, F) with *p ≤ 0.05; **p ≤ 0.01; ***p ≤ 0.005. ns, not significant. n.d., not detectable.

    Article Snippet: The following agonists/antagonists were used: acetylcholine chloride (10µM, AChR agonist, Merck, Darmstadt, Germany), nicotine (10µM, nAChR agonist, Merck, Darmstadt, Germany), muscarine chloride hydrate (10µM, mAChR agonist, Merck, Darmstadt, Germany), GTS-21 (100µM, a7nAChR agonist, Merck, Darmstadt, Germany), mecamylamine HCL (100µM, nAChR antagonist, Merck, Darmstadt, Germany), alpha-Bungarotoxin (100µM, a7nAChR antagonist, Alomone labs, Jerusalem, Israel), tyrphostin AG490 (1µM, blocking Janus kinase (Jak) 2, Merck, Darmstadt, Germany), and wortmannin (1µM, blocking phosphoinositide 3-kinase (PI3K), Merck, Darmstadt, Germany).

    Techniques: Expressing, MTS Assay