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muc5ac level (Cusabio)

Name: muc5ac level
Brand: Cusabio
Rating: 93 (6 reviews)

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Cusabio muc5ac level
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.

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.

Muc5ac Level, supplied by Cusabio, used in various techniques. Bioz Stars score: 93/100, based on 6 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 93 stars, based on 6 article reviews

muc5ac level - by Bioz Stars, 2026-03

93/100 stars

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1) Product Images from "Dictamnine Exhibits Anti-Asthmatic Effects by Modulating TGF-β/Smad2/3 Signaling in a Murine Asthma Model and Human Bronchial Epithelial Cells"

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

Journal: International Journal of Molecular Sciences

doi: 10.3390/ijms262411891

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.

Figure Legend 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.

Techniques Used:

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Figure 4. Effect of transfection with miR-708-5p mimic on FOXA2 expression and MUC5AC secretion by A549 epithelial cells. A549 cells were seeded on 24-well plates and transfected with miR-708-5p mimics or negative control siRNA (1 nM) in A549 cells in serum free medium. Cells were harvested for RNA isolation and cell-free supernatants were collected after 24 h. (a) Expression of FOXA2 was normalized to the housekeeping genes PPIA and B2M and compared between treatment with oligo control and miR-708-5p mimics. (b) MUC5AC levels were measured in cell-free supernatants by ELISA and compared between treatment with oligo control and miR-708-5p mimics. Four experiments were performed independently. Signiﬁcant differences were determined by paired Student’s t-test. * p < 0.05 between the indicated values.

Journal: Cells

Article Title: MicroRNAs Associated with Chronic Mucus Hypersecretion in COPD Are Involved in Fibroblast-Epithelium Crosstalk.

doi: 10.3390/cells11030526

Figure Lengend Snippet: Figure 4. Effect of transfection with miR-708-5p mimic on FOXA2 expression and MUC5AC secretion by A549 epithelial cells. A549 cells were seeded on 24-well plates and transfected with miR-708-5p mimics or negative control siRNA (1 nM) in A549 cells in serum free medium. Cells were harvested for RNA isolation and cell-free supernatants were collected after 24 h. (a) Expression of FOXA2 was normalized to the housekeeping genes PPIA and B2M and compared between treatment with oligo control and miR-708-5p mimics. (b) MUC5AC levels were measured in cell-free supernatants by ELISA and compared between treatment with oligo control and miR-708-5p mimics. Four experiments were performed independently. Signiﬁcant differences were determined by paired Student’s t-test. * p < 0.05 between the indicated values.

Article Snippet: Mucin 5AC (MUC5AC) levels were determined in supernatants using C96 Maxisorp NUNC Immuno-plate (Sigma-Aldrich, Darmstadt, Germany) coated with 100 μL/well of 500 ng/mL MUC5AC antibody (Thermo Fisher Scientific, Waltham, MA, USA) diluted in PBS (Gibco, California, CA, USA) overnight at room temperature on a platform shaker.

Techniques: Transfection, Expressing, Negative Control, Isolation, Control, Enzyme-linked Immunosorbent Assay

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:

Journal: International Journal of Chronic Obstructive Pulmonary Disease

Article Title: Effective-Component Compatibility of Bufei Yishen Formula (ECC-BYF) III Inhibits Mucus Hypersecretion by BEAS-2B Cells via miR-146a-5p-Mediated Regulation of the EGFR/MEK/ERK Pathway

doi: 10.2147/COPD.S498477

Figure Lengend Snippet: Primers Used in This Study

Article Snippet: The cell supernatants were collected to measure TNF-α levels (E-EL-H2306, Elabscience, China), and the cells were collected to measure MUC5AC (ELK2098, ELK Biotechnology, China) and MUC5B (ELK2122, ELK Biotechnology, China) levels.

Techniques: Sequencing, Negative Control

Screening of conditions to establish a model of mucus hypersecretion by BEAS-2B cells exposed to CSE. ( A ) Effects of different durations and concentrations of CSE on the proliferation of BEAS-2B cells. ( B and C ) Microscopic images of BEAS-2B cells treated with different concentrations of CSE (0%, 2.5%, 5%, 7.5%, 10%, 15%) for different times (6 h, 12 h, 24 h, 48 h) (×10). ( D and E ) Relative mRNA expression of MUC5AC and MUC5B in BEAS-2B cells after exposure to CSE for different durations and at different concentrations. ( F ) Relative protein expression of MUC5AC in BEAS-2B cells exposed to different concentrations of CSE for 12 h, 18 h and 24 h. All the data are presented as the means ± SDs (n = 3), a P < 0.05, aa P < 0.01 versus the control group.

Journal: International Journal of Chronic Obstructive Pulmonary Disease

doi: 10.2147/COPD.S498477

Figure Lengend Snippet: Screening of conditions to establish a model of mucus hypersecretion by BEAS-2B cells exposed to CSE. ( A ) Effects of different durations and concentrations of CSE on the proliferation of BEAS-2B cells. ( B and C ) Microscopic images of BEAS-2B cells treated with different concentrations of CSE (0%, 2.5%, 5%, 7.5%, 10%, 15%) for different times (6 h, 12 h, 24 h, 48 h) (×10). ( D and E ) Relative mRNA expression of MUC5AC and MUC5B in BEAS-2B cells after exposure to CSE for different durations and at different concentrations. ( F ) Relative protein expression of MUC5AC in BEAS-2B cells exposed to different concentrations of CSE for 12 h, 18 h and 24 h. All the data are presented as the means ± SDs (n = 3), a P < 0.05, aa P < 0.01 versus the control group.

Techniques: Expressing, Control

The optimal intervention concentration of ECC-BYF III was screened. ( A ) Effects of different durations and concentrations of ECC-BYF III on the proliferation of BEAS-2B cells. All the data are presented as the means ± SDs (n =3), a P < 0.05, aa P < 0.01 versus the control group. ( B and C ) Relative mRNA expression of MUC5AC and MUC5B in BEAS-2B cells exposed to 5% CSE or 10% CSE in the ECC-BYF III low-, medium- and high-dose groups. All the data are presented as the means ± SDs (n =3), a P < 0.05, aa P < 0.01 versus the control group. b P < 0.05, bb P < 0.01 versus the model group. c P < 0.05, cc P < 0.01 versus the ECC-BYF III -M group. ( D and E ) Relative protein expression of MUC5AC in BEAS-2B cells exposed to 5% CSE and 10% CSE in the ECC-BYF III low-, medium- and high-dose groups. All the data are presented as the means ± SDs (n =3), a P < 0.05, aa P < 0.01 versus the control group. b P < 0.05, bb P < 0.01 versus the model group. c P < 0.05, cc P < 0.01 versus the ECC-BYF III-L group.

Journal: International Journal of Chronic Obstructive Pulmonary Disease

doi: 10.2147/COPD.S498477

Figure Lengend Snippet: The optimal intervention concentration of ECC-BYF III was screened. ( A ) Effects of different durations and concentrations of ECC-BYF III on the proliferation of BEAS-2B cells. All the data are presented as the means ± SDs (n =3), a P < 0.05, aa P < 0.01 versus the control group. ( B and C ) Relative mRNA expression of MUC5AC and MUC5B in BEAS-2B cells exposed to 5% CSE or 10% CSE in the ECC-BYF III low-, medium- and high-dose groups. All the data are presented as the means ± SDs (n =3), a P < 0.05, aa P < 0.01 versus the control group. b P < 0.05, bb P < 0.01 versus the model group. c P < 0.05, cc P < 0.01 versus the ECC-BYF III -M group. ( D and E ) Relative protein expression of MUC5AC in BEAS-2B cells exposed to 5% CSE and 10% CSE in the ECC-BYF III low-, medium- and high-dose groups. All the data are presented as the means ± SDs (n =3), a P < 0.05, aa P < 0.01 versus the control group. b P < 0.05, bb P < 0.01 versus the model group. c P < 0.05, cc P < 0.01 versus the ECC-BYF III-L group.

Techniques: Concentration Assay, Control, Expressing

ECC-BYF III can ameliorate mucus hypersecretion and affect the levels of inflammatory factors, miR-146a-5p and EGFR/MEK/ERK pathway components. ( A and B ) Relative protein expression of MUC5AC and MUC5B in each group. ( C ) Relative mRNA expression of IL-4, IL-1α, IL-8 and TNF-α in each group. ( D ) Relative protein expression of TNF-α in each group. ( E and F ) Relative mRNA expression of miR-146a-5p, MUC5AC and MUC5B in each group. ( G – K ) Expression of EGFR/MEK/ERK pathway-related proteins affected by ECC-BYF III. All the data are presented as the mean ± SDs (n =3), a P < 0.05, aa P < 0.01 versus the control group. b P < 0.05, bb P < 0.01 versus the model group.

Journal: International Journal of Chronic Obstructive Pulmonary Disease

doi: 10.2147/COPD.S498477

Figure Lengend Snippet: ECC-BYF III can ameliorate mucus hypersecretion and affect the levels of inflammatory factors, miR-146a-5p and EGFR/MEK/ERK pathway components. ( A and B ) Relative protein expression of MUC5AC and MUC5B in each group. ( C ) Relative mRNA expression of IL-4, IL-1α, IL-8 and TNF-α in each group. ( D ) Relative protein expression of TNF-α in each group. ( E and F ) Relative mRNA expression of miR-146a-5p, MUC5AC and MUC5B in each group. ( G – K ) Expression of EGFR/MEK/ERK pathway-related proteins affected by ECC-BYF III. All the data are presented as the mean ± SDs (n =3), a P < 0.05, aa P < 0.01 versus the control group. b P < 0.05, bb P < 0.01 versus the model group.

Techniques: Expressing, Control

Effects of miR-146a-5p overexpression on MUC5AC, MUC5B and the EGFR/MEK/ERK pathway. ( A and B ) The relative mRNA expression levels of miR-146a-5p, MUC5AC and MUC5B in each group after transfection. ( C ) Protein expression of MUC5AC after transfection. All the data are presented as the means ± SDs (n = 3). NC Control group compared with NC Model group, aa P < 0.01; NC Control group compared with mimic Control group, bb P < 0.01; NC Model group compared with mimic Model group, c P < 0.05, cc P < 0.01. ( D – G ) Effect of miR-146a-5p overexpression on the EGFR/MEK/ERK pathway. All the data are presented as the means ± SDs (n =3). Mimic Control group compared with NC Control group, a P < 0.05, aa P < 0.01; NC Control group compared with NC Model group, b P < 0.05, bb P < 0.01; NC Model group compared with mimic Model group, c P < 0.05, cc P < 0.01.

Journal: International Journal of Chronic Obstructive Pulmonary Disease

doi: 10.2147/COPD.S498477

Figure Lengend Snippet: Effects of miR-146a-5p overexpression on MUC5AC, MUC5B and the EGFR/MEK/ERK pathway. ( A and B ) The relative mRNA expression levels of miR-146a-5p, MUC5AC and MUC5B in each group after transfection. ( C ) Protein expression of MUC5AC after transfection. All the data are presented as the means ± SDs (n = 3). NC Control group compared with NC Model group, aa P < 0.01; NC Control group compared with mimic Control group, bb P < 0.01; NC Model group compared with mimic Model group, c P < 0.05, cc P < 0.01. ( D – G ) Effect of miR-146a-5p overexpression on the EGFR/MEK/ERK pathway. All the data are presented as the means ± SDs (n =3). Mimic Control group compared with NC Control group, a P < 0.05, aa P < 0.01; NC Control group compared with NC Model group, b P < 0.05, bb P < 0.01; NC Model group compared with mimic Model group, c P < 0.05, cc P < 0.01.

Techniques: Over Expression, Expressing, Transfection, Control

Effects of miR-146a-5p downregulation on the ability of ECC-BYF III to regulate mucus hypersecretion and the EGFR/MEK/ERK pathway in BEAS-2B cells. ( A and B ) Relative mRNA expression of miR-146a-5p, MUC5AC and MUC5B in each group after transfection. ( C ) Protein expression of MUC5AC after transfection. ( D – G ) Effect of downregulating miR-146a-5p on the EGFR/MRK/ERK pathway. All the data are presented as the means ± SDs (n =3). IN NC Control group compared with IN NC Model group, aa P < 0.01; IN NC Model group compared with IN NC ECC-BYF III group, b P < 0.05, bb P < 0.01; IN NC ECC-BYF III group compared with IN ECC-BYF III group, cc P < 0.01.

Journal: International Journal of Chronic Obstructive Pulmonary Disease

doi: 10.2147/COPD.S498477

Figure Lengend Snippet: Effects of miR-146a-5p downregulation on the ability of ECC-BYF III to regulate mucus hypersecretion and the EGFR/MEK/ERK pathway in BEAS-2B cells. ( A and B ) Relative mRNA expression of miR-146a-5p, MUC5AC and MUC5B in each group after transfection. ( C ) Protein expression of MUC5AC after transfection. ( D – G ) Effect of downregulating miR-146a-5p on the EGFR/MRK/ERK pathway. All the data are presented as the means ± SDs (n =3). IN NC Control group compared with IN NC Model group, aa P < 0.01; IN NC Model group compared with IN NC ECC-BYF III group, b P < 0.05, bb P < 0.01; IN NC ECC-BYF III group compared with IN ECC-BYF III group, cc P < 0.01.

Techniques: Expressing, Transfection, Control

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

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1) Product Images from "Dictamnine Exhibits Anti-Asthmatic Effects by Modulating TGF-β/Smad2/3 Signaling in a Murine Asthma Model and Human Bronchial Epithelial Cells"

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