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elisa kit nbp2 76704  (Novus Biologicals)


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    Novus Biologicals elisa kit nbp2 76704
    Elisa Kit Nbp2 76704, supplied by Novus Biologicals, used in various techniques. Bioz Stars score: 93/100, based on 9 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/elisa kit nbp2 76704/product/Novus Biologicals
    Average 93 stars, based on 9 article reviews
    elisa kit nbp2 76704 - by Bioz Stars, 2026-03
    93/100 stars

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    Dictamnine reduced Th2 cytokine, <t>MUC5AC,</t> and OVA-specific IgE levels in OVA-induced asthmatic mice. ( a – c ) BALF cytokine levels: ( a ) IL-4, ( b ) IL-5, and ( c ) IL-13. ( d ) MUC5AC levels in BALF. ( e ) OVA-specific IgE levels in serum. Data are expressed as mean ± SEM ( n = 5 per group). * p < 0.05, ** p < 0.01, and *** p < 0.001 compared to the AC group.
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    Novus Biologicals muc5ac concentrations
    Plexin B1 regulates mucin expression in lungs. BALF was evaluated for <t>MUC5AC</t> by ELISA, n=7 mice/group (A) . (B) Lung RNA was isolated from the indicated mice and evaluated for mucin gene expression by qRT-PCR as described in Materials and Methods (n=4-8/group). Data shown as mean ± SEM (A, B) with data statistics calculated using two-way ANOVA with Tukey’s multiple comparison test.
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    Cusabio muc5ac levels
    Fig. 1. GPR120 agonist alleviates allergic airway inflammation and mucin secretion in OVA-induced asthmatic mice. Schematic overview of OVA-induced asthma experiment. Mice were sensitized and challenged with OVA and were intraperitoneally treated with vehicle, 20 mg/kg/day of GSK137647A, a GPR120 agonist or 5 mg/kg/day of dexamethasone (DEX). (B) Hematoxylin and eosin (H&E) staining of lung tissue sections. Infiltration of inflammatory cells in peribronchiolar regions (arrowheads). Scale bar: 100 µm. (C) Histopathological scores of peribronchiolar inflammatory cell infiltration. (D) Inflammatory cell counts in the bronchoalveolar lavage fluid (BALF). (E) Spleen to body weight ratio. (F) Mucin production in bronchiolar epithelial goblet cells stained with Periodic Acid-Schiff (PAS). Scale bar: 100 µm. (G) Histopathological scores of PAS-stained mucin production in bronchiolar epithelial goblet cells. (H) Levels of <t>MUC5AC</t> secretion in BALF measured by ELISA. (I) Representative Western blot analysis images of GPR120 protein expression in lung tissue samples (3 independent sets of experiment). (J) Densitometry values of GPR120 expression in the lung tissue samples. (n = 3–6 per condition; *P < 0.05; **P < 0.01, compared with control. #P < 0.05; ##P < 0.01; ###P < 0.001, compared with OVA-challenged group; ANOVA with Bonferroni multiple comparison test.).
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    Image Search Results


    Dictamnine reduced Th2 cytokine, MUC5AC, and OVA-specific IgE levels in OVA-induced asthmatic mice. ( a – c ) BALF cytokine levels: ( a ) IL-4, ( b ) IL-5, and ( c ) IL-13. ( d ) MUC5AC levels in BALF. ( e ) OVA-specific IgE levels in serum. Data are expressed as mean ± SEM ( n = 5 per group). * p < 0.05, ** p < 0.01, and *** p < 0.001 compared to the AC group.

    Journal: International Journal of Molecular Sciences

    Article Title: Dictamnine Exhibits Anti-Asthmatic Effects by Modulating TGF-β/Smad2/3 Signaling in a Murine Asthma Model and Human Bronchial Epithelial Cells

    doi: 10.3390/ijms262411891

    Figure Lengend Snippet: Dictamnine reduced Th2 cytokine, MUC5AC, and OVA-specific IgE levels in OVA-induced asthmatic mice. ( a – c ) BALF cytokine levels: ( a ) IL-4, ( b ) IL-5, and ( c ) IL-13. ( d ) MUC5AC levels in BALF. ( e ) OVA-specific IgE levels in serum. Data are expressed as mean ± SEM ( n = 5 per group). * p < 0.05, ** p < 0.01, and *** p < 0.001 compared to the AC group.

    Article Snippet: MUC5AC level in BALF was determined using the Mouse MUC5AC ELISA kit (CSB-E11040m; Cusabio, Wuhan, China).

    Techniques:

    Dictamnine reduced Th2 cytokine, MUC5AC, and OVA-specific IgE levels in OVA-induced asthmatic mice. ( a – c ) BALF cytokine levels: ( a ) IL-4, ( b ) IL-5, and ( c ) IL-13. ( d ) MUC5AC levels in BALF. ( e ) OVA-specific IgE levels in serum. Data are expressed as mean ± SEM ( n = 5 per group). * p < 0.05, ** p < 0.01, and *** p < 0.001 compared to the AC group.

    Journal: International Journal of Molecular Sciences

    Article Title: Dictamnine Exhibits Anti-Asthmatic Effects by Modulating TGF-β/Smad2/3 Signaling in a Murine Asthma Model and Human Bronchial Epithelial Cells

    doi: 10.3390/ijms262411891

    Figure Lengend Snippet: Dictamnine reduced Th2 cytokine, MUC5AC, and OVA-specific IgE levels in OVA-induced asthmatic mice. ( a – c ) BALF cytokine levels: ( a ) IL-4, ( b ) IL-5, and ( c ) IL-13. ( d ) MUC5AC levels in BALF. ( e ) OVA-specific IgE levels in serum. Data are expressed as mean ± SEM ( n = 5 per group). * p < 0.05, ** p < 0.01, and *** p < 0.001 compared to the AC group.

    Article Snippet: MUC5AC level in BALF was determined using the Mouse MUC5AC ELISA kit (CSB-E11040m; Cusabio, Wuhan, China).

    Techniques:

    Plexin B1 regulates mucin expression in lungs. BALF was evaluated for MUC5AC by ELISA, n=7 mice/group (A) . (B) Lung RNA was isolated from the indicated mice and evaluated for mucin gene expression by qRT-PCR as described in Materials and Methods (n=4-8/group). Data shown as mean ± SEM (A, B) with data statistics calculated using two-way ANOVA with Tukey’s multiple comparison test.

    Journal: Frontiers in Immunology

    Article Title: Plexin B1 controls Treg numbers, limits allergic airway inflammation, and regulates mucins

    doi: 10.3389/fimmu.2023.1297354

    Figure Lengend Snippet: Plexin B1 regulates mucin expression in lungs. BALF was evaluated for MUC5AC by ELISA, n=7 mice/group (A) . (B) Lung RNA was isolated from the indicated mice and evaluated for mucin gene expression by qRT-PCR as described in Materials and Methods (n=4-8/group). Data shown as mean ± SEM (A, B) with data statistics calculated using two-way ANOVA with Tukey’s multiple comparison test.

    Article Snippet: The Muc5AC concentrations in BALF were determined with the use of ELISA kit NBP2-76704 (Novus Biologicals) according to the manufacturer’s instruction.

    Techniques: Expressing, Enzyme-linked Immunosorbent Assay, Isolation, Gene Expression, Quantitative RT-PCR, Comparison

    Fig. 1. GPR120 agonist alleviates allergic airway inflammation and mucin secretion in OVA-induced asthmatic mice. Schematic overview of OVA-induced asthma experiment. Mice were sensitized and challenged with OVA and were intraperitoneally treated with vehicle, 20 mg/kg/day of GSK137647A, a GPR120 agonist or 5 mg/kg/day of dexamethasone (DEX). (B) Hematoxylin and eosin (H&E) staining of lung tissue sections. Infiltration of inflammatory cells in peribronchiolar regions (arrowheads). Scale bar: 100 µm. (C) Histopathological scores of peribronchiolar inflammatory cell infiltration. (D) Inflammatory cell counts in the bronchoalveolar lavage fluid (BALF). (E) Spleen to body weight ratio. (F) Mucin production in bronchiolar epithelial goblet cells stained with Periodic Acid-Schiff (PAS). Scale bar: 100 µm. (G) Histopathological scores of PAS-stained mucin production in bronchiolar epithelial goblet cells. (H) Levels of MUC5AC secretion in BALF measured by ELISA. (I) Representative Western blot analysis images of GPR120 protein expression in lung tissue samples (3 independent sets of experiment). (J) Densitometry values of GPR120 expression in the lung tissue samples. (n = 3–6 per condition; *P < 0.05; **P < 0.01, compared with control. #P < 0.05; ##P < 0.01; ###P < 0.001, compared with OVA-challenged group; ANOVA with Bonferroni multiple comparison test.).

    Journal: Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie

    Article Title: GPR120/FFAR4 stimulation attenuates airway remodeling and suppresses IL-4- and IL-13-induced airway epithelial injury via inhibition of STAT6 and Akt.

    doi: 10.1016/j.biopha.2023.115774

    Figure Lengend Snippet: Fig. 1. GPR120 agonist alleviates allergic airway inflammation and mucin secretion in OVA-induced asthmatic mice. Schematic overview of OVA-induced asthma experiment. Mice were sensitized and challenged with OVA and were intraperitoneally treated with vehicle, 20 mg/kg/day of GSK137647A, a GPR120 agonist or 5 mg/kg/day of dexamethasone (DEX). (B) Hematoxylin and eosin (H&E) staining of lung tissue sections. Infiltration of inflammatory cells in peribronchiolar regions (arrowheads). Scale bar: 100 µm. (C) Histopathological scores of peribronchiolar inflammatory cell infiltration. (D) Inflammatory cell counts in the bronchoalveolar lavage fluid (BALF). (E) Spleen to body weight ratio. (F) Mucin production in bronchiolar epithelial goblet cells stained with Periodic Acid-Schiff (PAS). Scale bar: 100 µm. (G) Histopathological scores of PAS-stained mucin production in bronchiolar epithelial goblet cells. (H) Levels of MUC5AC secretion in BALF measured by ELISA. (I) Representative Western blot analysis images of GPR120 protein expression in lung tissue samples (3 independent sets of experiment). (J) Densitometry values of GPR120 expression in the lung tissue samples. (n = 3–6 per condition; *P < 0.05; **P < 0.01, compared with control. #P < 0.05; ##P < 0.01; ###P < 0.001, compared with OVA-challenged group; ANOVA with Bonferroni multiple comparison test.).

    Article Snippet: MUC5AC levels in BALF were determined by ELISA (CSB-E11040m; Cusabio, Houston, TX, USA), according to the manufacturer’s instructions.

    Techniques: Staining, Enzyme-linked Immunosorbent Assay, Western Blot, Expressing, Control, Comparison

    Fig. 2. GPR120 inhibits IL-4- and IL-13-induced production of MUC5AC and cytokines in 16HBE human bronchial epithelial cells. 16HBE monolayers were incu bated with 10 ng/mL each of IL-4 and IL-13 and co-treated with or without 1 µM of GSK137647A for 48 h. To confirm activation of GPR120, cells were pretreated with 100 µM of AH7614, GPR120 antagonist for 1 h before the experiment. (A) Representative Western blot analysis images of GPR120 expression (3 independent sets of experiment). (B) Expression of MUC5AC (green) as depicted by immunofluorescent staining. Scale bar: 50 µm. (C) Fluorescent intensity ratio (MUC5AC to nuclei). (D) mRNA expression of MUC5AC. (E) Expression of cytokine transcripts IL6, IL8, IL25, and TSLP. (ns, non-significant difference; *P < 0.05; **P < 0.01, ***P < 0.001; ANOVA with Bonferroni multiple comparison test. n = 6–7 per condition.).

    Journal: Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie

    Article Title: GPR120/FFAR4 stimulation attenuates airway remodeling and suppresses IL-4- and IL-13-induced airway epithelial injury via inhibition of STAT6 and Akt.

    doi: 10.1016/j.biopha.2023.115774

    Figure Lengend Snippet: Fig. 2. GPR120 inhibits IL-4- and IL-13-induced production of MUC5AC and cytokines in 16HBE human bronchial epithelial cells. 16HBE monolayers were incu bated with 10 ng/mL each of IL-4 and IL-13 and co-treated with or without 1 µM of GSK137647A for 48 h. To confirm activation of GPR120, cells were pretreated with 100 µM of AH7614, GPR120 antagonist for 1 h before the experiment. (A) Representative Western blot analysis images of GPR120 expression (3 independent sets of experiment). (B) Expression of MUC5AC (green) as depicted by immunofluorescent staining. Scale bar: 50 µm. (C) Fluorescent intensity ratio (MUC5AC to nuclei). (D) mRNA expression of MUC5AC. (E) Expression of cytokine transcripts IL6, IL8, IL25, and TSLP. (ns, non-significant difference; *P < 0.05; **P < 0.01, ***P < 0.001; ANOVA with Bonferroni multiple comparison test. n = 6–7 per condition.).

    Article Snippet: MUC5AC levels in BALF were determined by ELISA (CSB-E11040m; Cusabio, Houston, TX, USA), according to the manufacturer’s instructions.

    Techniques: Activation Assay, Western Blot, Expressing, Staining, Comparison

    Fig. 7. Schematic diagram demonstrating mechanisms by which GPR120 stimulation suppresses cytokine-induced airway remodeling in asthmatic models. Acti vation of type-I IL-4R (IL4Rα/γ-chain dimerization) emanates signaling via activation of insulin receptor substrate (IRS)-phosphoinositide 3-kinase (PI3K)-Akt pathway and JAK-STAT6 pathway, while type-II IL-4R (IL-4Rα/IL-13Rα1 dimerization) activates JAK-STAT6 pathway. GPR120 stimulation by GSK137647A at tenuates airway epithelial remodeling hallmarks including increased MUC5AC, tight junction disruption, and upregulated fibrotic markers. GPR120 stimulation attenuates the epithelial disrupting effects of IL-4 and IL-13 signaling via inhibition of STAT6 and Akt.

    Journal: Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie

    Article Title: GPR120/FFAR4 stimulation attenuates airway remodeling and suppresses IL-4- and IL-13-induced airway epithelial injury via inhibition of STAT6 and Akt.

    doi: 10.1016/j.biopha.2023.115774

    Figure Lengend Snippet: Fig. 7. Schematic diagram demonstrating mechanisms by which GPR120 stimulation suppresses cytokine-induced airway remodeling in asthmatic models. Acti vation of type-I IL-4R (IL4Rα/γ-chain dimerization) emanates signaling via activation of insulin receptor substrate (IRS)-phosphoinositide 3-kinase (PI3K)-Akt pathway and JAK-STAT6 pathway, while type-II IL-4R (IL-4Rα/IL-13Rα1 dimerization) activates JAK-STAT6 pathway. GPR120 stimulation by GSK137647A at tenuates airway epithelial remodeling hallmarks including increased MUC5AC, tight junction disruption, and upregulated fibrotic markers. GPR120 stimulation attenuates the epithelial disrupting effects of IL-4 and IL-13 signaling via inhibition of STAT6 and Akt.

    Article Snippet: MUC5AC levels in BALF were determined by ELISA (CSB-E11040m; Cusabio, Houston, TX, USA), according to the manufacturer’s instructions.

    Techniques: Activation Assay, Disruption, Inhibition