mouse il-1β Search Results


  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
  • 86
    Millipore il 1β
    siRNA knock down of NLRP3 prevents LPS-induced caspase-1 activation and <t>IL-1β</t> production by cardiac fibroblasts (CFs). CFs were transfected with siRNA specific to NLRP3 or with scrambled siRNA. Forty eight hrs after transfection, the cells were challenged with LPS (1 µg/ml) or vehicle for 24 hrs. The cells were lysed for the detection of intracellular NLRP3 ( A ), caspase-1 p10 ( B ), and intracellular IL-1β ( C ) with Western blot. The supernatants were harvested for the detection of released IL-1β with ELISA ( D ). For A , B , and C , representative blots and densitometric analyses are shown. n = 3 for all experiments (A–D). *p
    Il 1β, supplied by Millipore, 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/il 1β/product/Millipore
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    il 1β - by Bioz Stars, 2021-05
    86/100 stars
      Buy from Supplier

    99
    PeproTech il 1β
    Exosome‐delivered mesenchymal‐epithelial transition factor (MET) stimulates macrophages to facilitate tumour growth in vivo. A, The effects of the supernatant from macrophage treated with PBS, MET + exosomes, MET − exosomes, MET − exosomes + recombinant <t>IL‐1β</t> protein, MET + exosomes + IL‐1β neutralizing antibody on tumour growth in a xenograft model. Tumour volume in the xenograft models was measured every 3 d after a 10 d inoculation period. B,C, Final tumour weights were determined and photographed. * P
    Il 1β, supplied by PeproTech, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/il 1β/product/PeproTech
    Average 99 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    il 1β - by Bioz Stars, 2021-05
    99/100 stars
      Buy from Supplier

    96
    R&D Systems il 1β
    Effects of HG on the secretion of <t>IL-1β</t> and IL-18 in HPMCs. HPMCs were treated with 76, 126 and 214 mM glucose for 6, 12, 24 and 48 h. The levels of (A) IL-18 and (B) IL-1β in the supernatant were detected using enzyme-linked immunosorbent
    Il 1β, supplied by R&D Systems, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/il 1β/product/R&D Systems
    Average 96 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    il 1β - by Bioz Stars, 2021-05
    96/100 stars
      Buy from Supplier

    99
    Cell Signaling Technology Inc il 1β
    Recombinant human interleukin-1 receptor antagonist (RhIL-1Ra) ameliorated ConA-induced NOD-like receptor protein 3 (NLRP3) inflammasome activation and pyroptosis. (A) BALB/c mice ( n = 6 for each group) were pretreated with rhIL-1Ra before ConA injection, and samples were extracted at 12 h post ConA treatment. Serum <t>IL-1β</t> and IL-18 were detected by ELISA. (B) Liver homogenates were subjected to caspase-1 activity assay. (C) Western blot of NLRP3, Cleaved caspase-1, and IL-1β in the livers. GAPDH acted as a loading control. Each lane represented a separate animal. Results were obtained from three experiments. Quantification of protein expression were obtained by Image J software. (D) Caspase-1 positive death cells staining were observed by confocal microscopy. FAM-YVAD-FMK (green), propidium iodide (red), Hoechst 33342 (blue). The data were presented as means ± SD (Student’s t -test, * p
    Il 1β, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/il 1β/product/Cell Signaling Technology Inc
    Average 99 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    il 1β - by Bioz Stars, 2021-05
    99/100 stars
      Buy from Supplier




    N/A
    The IL 1 family consists primarily of three proteins IL 1α IL 1β agonists and IL 1ra antagonist which interact with the IL 1 receptor IL 1β shares 33 homology
      Buy from Supplier

    Image Search Results


    siRNA knock down of NLRP3 prevents LPS-induced caspase-1 activation and IL-1β production by cardiac fibroblasts (CFs). CFs were transfected with siRNA specific to NLRP3 or with scrambled siRNA. Forty eight hrs after transfection, the cells were challenged with LPS (1 µg/ml) or vehicle for 24 hrs. The cells were lysed for the detection of intracellular NLRP3 ( A ), caspase-1 p10 ( B ), and intracellular IL-1β ( C ) with Western blot. The supernatants were harvested for the detection of released IL-1β with ELISA ( D ). For A , B , and C , representative blots and densitometric analyses are shown. n = 3 for all experiments (A–D). *p

    Journal: PLoS ONE

    Article Title: Cardiac Fibroblasts Contribute to Myocardial Dysfunction in Mice with Sepsis: The Role of NLRP3 Inflammasome Activation

    doi: 10.1371/journal.pone.0107639

    Figure Lengend Snippet: siRNA knock down of NLRP3 prevents LPS-induced caspase-1 activation and IL-1β production by cardiac fibroblasts (CFs). CFs were transfected with siRNA specific to NLRP3 or with scrambled siRNA. Forty eight hrs after transfection, the cells were challenged with LPS (1 µg/ml) or vehicle for 24 hrs. The cells were lysed for the detection of intracellular NLRP3 ( A ), caspase-1 p10 ( B ), and intracellular IL-1β ( C ) with Western blot. The supernatants were harvested for the detection of released IL-1β with ELISA ( D ). For A , B , and C , representative blots and densitometric analyses are shown. n = 3 for all experiments (A–D). *p

    Article Snippet: The potential role of IL-1β on cAMP accumulation was studied by adding IL-1β (5 ng/mL) (Millipore, Billerica, MA, USA) to naïve cardiomyocytes as indicated.

    Techniques: Activation Assay, Transfection, Western Blot, Enzyme-linked Immunosorbent Assay

    Sepsis-induced increases in myocardial and circulating IL-1β is reduced by inhibition of the NLRP3 inflammasome. Polymicrobial sepsis (FIP) was induced by i.p. injection of 0.5 ml of fecal material (30 mg/ml). Myocardial tissue was harvested for measurement (Western blot) of NLRP3, pro-caspase-1, activated caspase-1 p10, and pro-IL-1β. Representative Westerns are shown in panel A and densitometric analyses in panels B-E. Mature (activated) IL-1β in myocardial homogenates and plasma assessed with ELISA, panels F and G, respectively. n = 5 for all experiments; *p

    Journal: PLoS ONE

    Article Title: Cardiac Fibroblasts Contribute to Myocardial Dysfunction in Mice with Sepsis: The Role of NLRP3 Inflammasome Activation

    doi: 10.1371/journal.pone.0107639

    Figure Lengend Snippet: Sepsis-induced increases in myocardial and circulating IL-1β is reduced by inhibition of the NLRP3 inflammasome. Polymicrobial sepsis (FIP) was induced by i.p. injection of 0.5 ml of fecal material (30 mg/ml). Myocardial tissue was harvested for measurement (Western blot) of NLRP3, pro-caspase-1, activated caspase-1 p10, and pro-IL-1β. Representative Westerns are shown in panel A and densitometric analyses in panels B-E. Mature (activated) IL-1β in myocardial homogenates and plasma assessed with ELISA, panels F and G, respectively. n = 5 for all experiments; *p

    Article Snippet: The potential role of IL-1β on cAMP accumulation was studied by adding IL-1β (5 ng/mL) (Millipore, Billerica, MA, USA) to naïve cardiomyocytes as indicated.

    Techniques: Inhibition, Injection, Western Blot, Enzyme-linked Immunosorbent Assay

    Inhibition of the NLRP3 inflammasome prevents LPS-induced increase in myocardial and circulating IL-1β in mice. Mice were injected (i.p.) with saline (sham), LPS (10 mg/kg), LPS with glyburide (1 mg/Kg), or glyburide alone. Eight hours later, myocardial tissue was harvested for measurement (Western blot) of NLRP3, pro-caspase-1, activated caspase-1p10, pro-IL-1β and IL-1β. Representative Westerns shown in panel A and densitometric analyses in panels B–F. Mature (activated) Il-1β in myocardial homogenates and plasma assessed with ELISA, panels F and G, respectively. n = 5 for all experiments; *p

    Journal: PLoS ONE

    Article Title: Cardiac Fibroblasts Contribute to Myocardial Dysfunction in Mice with Sepsis: The Role of NLRP3 Inflammasome Activation

    doi: 10.1371/journal.pone.0107639

    Figure Lengend Snippet: Inhibition of the NLRP3 inflammasome prevents LPS-induced increase in myocardial and circulating IL-1β in mice. Mice were injected (i.p.) with saline (sham), LPS (10 mg/kg), LPS with glyburide (1 mg/Kg), or glyburide alone. Eight hours later, myocardial tissue was harvested for measurement (Western blot) of NLRP3, pro-caspase-1, activated caspase-1p10, pro-IL-1β and IL-1β. Representative Westerns shown in panel A and densitometric analyses in panels B–F. Mature (activated) Il-1β in myocardial homogenates and plasma assessed with ELISA, panels F and G, respectively. n = 5 for all experiments; *p

    Article Snippet: The potential role of IL-1β on cAMP accumulation was studied by adding IL-1β (5 ng/mL) (Millipore, Billerica, MA, USA) to naïve cardiomyocytes as indicated.

    Techniques: Inhibition, Mouse Assay, Injection, Western Blot, Enzyme-linked Immunosorbent Assay

    Supernatants from LPS-challenged cardiac fibroblasts (CFs) can inhibit the increase in cardiomyocyte (CM) cAMP induced by dobutamine; an effect dependent on an intact NLRP3 inflammasome/IL-1β axis in CFs. In panels A–C, CM were challenged with supernatants from LPS- or vehicle- conditioned CFs.(CF→CM). In Panel A, the CFs were transfected with NLRP3 siRNA or glyburide (200 µM) prior to challenge with LPS for 24 hrs. Subsequently, the supernatants were added to CM monolayers and thereafter, the cardiomyocytes were stimulated with vehicle or dobutamine (7.5 µM) for 10 min. The CM were harvested for the measurement of intracellular cAMP. In Panel B, CM were challenged with supernatants from LPS- or vehicle- conditioned CFs, with or without IL-1Ra (5 µg/ml) and intracellular cAMP assessed after dobutamine treatment. In panel C, CM were challenged with IL-1β (5 ng/mL) or IL-1β plus IL-1Ra (5 µg/mL) for 24 hrs. Subsequently, the CM were challenged with dobutamine and cAMP of CM was assessed. For all experiments, n = 3 and *, #, +p

    Journal: PLoS ONE

    Article Title: Cardiac Fibroblasts Contribute to Myocardial Dysfunction in Mice with Sepsis: The Role of NLRP3 Inflammasome Activation

    doi: 10.1371/journal.pone.0107639

    Figure Lengend Snippet: Supernatants from LPS-challenged cardiac fibroblasts (CFs) can inhibit the increase in cardiomyocyte (CM) cAMP induced by dobutamine; an effect dependent on an intact NLRP3 inflammasome/IL-1β axis in CFs. In panels A–C, CM were challenged with supernatants from LPS- or vehicle- conditioned CFs.(CF→CM). In Panel A, the CFs were transfected with NLRP3 siRNA or glyburide (200 µM) prior to challenge with LPS for 24 hrs. Subsequently, the supernatants were added to CM monolayers and thereafter, the cardiomyocytes were stimulated with vehicle or dobutamine (7.5 µM) for 10 min. The CM were harvested for the measurement of intracellular cAMP. In Panel B, CM were challenged with supernatants from LPS- or vehicle- conditioned CFs, with or without IL-1Ra (5 µg/ml) and intracellular cAMP assessed after dobutamine treatment. In panel C, CM were challenged with IL-1β (5 ng/mL) or IL-1β plus IL-1Ra (5 µg/mL) for 24 hrs. Subsequently, the CM were challenged with dobutamine and cAMP of CM was assessed. For all experiments, n = 3 and *, #, +p

    Article Snippet: The potential role of IL-1β on cAMP accumulation was studied by adding IL-1β (5 ng/mL) (Millipore, Billerica, MA, USA) to naïve cardiomyocytes as indicated.

    Techniques: Transfection

    Treatment of cardiac fibroblasts (CFs) with LPS activates the NLRP3 inflammasome and results in the maturation (activation) and release of IL-1β. Mouse CFs were challenged with LPS (1 µg/ml) or saline (control). At the times indicated, the CFs were collected, lysed, and processed for the measurement (Western blot) of intracellular NLRP3 (A), pro-caspase-1 (B), activated caspase-1 p10 (C), pro-IL-1β (D), and IL-1β (E). Released IL-1β was also assessed by ELISA of the supernatants (F). For A through E, representative blots and densitometric analyses are shown. n = 3 for all experiments (A–F), *p

    Journal: PLoS ONE

    Article Title: Cardiac Fibroblasts Contribute to Myocardial Dysfunction in Mice with Sepsis: The Role of NLRP3 Inflammasome Activation

    doi: 10.1371/journal.pone.0107639

    Figure Lengend Snippet: Treatment of cardiac fibroblasts (CFs) with LPS activates the NLRP3 inflammasome and results in the maturation (activation) and release of IL-1β. Mouse CFs were challenged with LPS (1 µg/ml) or saline (control). At the times indicated, the CFs were collected, lysed, and processed for the measurement (Western blot) of intracellular NLRP3 (A), pro-caspase-1 (B), activated caspase-1 p10 (C), pro-IL-1β (D), and IL-1β (E). Released IL-1β was also assessed by ELISA of the supernatants (F). For A through E, representative blots and densitometric analyses are shown. n = 3 for all experiments (A–F), *p

    Article Snippet: The potential role of IL-1β on cAMP accumulation was studied by adding IL-1β (5 ng/mL) (Millipore, Billerica, MA, USA) to naïve cardiomyocytes as indicated.

    Techniques: Activation Assay, Western Blot, Enzyme-linked Immunosorbent Assay

    Inhibition of the NLRP3 inflammasome with glyburide (Glyb) prevents caspase-1 activation and IL-1β production by LPS-challenged cardiac fibroblasts (CFs). CFs were pretreated with either vehicle or glyburide (50 µM or 200 µM) 30 min before the LPS (1 µg/ml) challenge. Twenty-four hrs after LPS stimulation, the cells were harvested and processed for the measurement (Western blot) of intracellular NLRP3 (A), pro-caspase-1 (B), activated caspase-1 p10 (C), pro-IL-1β (D), and mature IL-1β (E). The supernatants were harvested for the detection of released IL-1β with ELISA (F). The basal levels of the various components of the NLRP3 inflammasome/IL-1β axis were not affected by glyburide. For A through E, representative blots and densitometric analyses are shown. n = 3 for all experiments (A–F). *p

    Journal: PLoS ONE

    Article Title: Cardiac Fibroblasts Contribute to Myocardial Dysfunction in Mice with Sepsis: The Role of NLRP3 Inflammasome Activation

    doi: 10.1371/journal.pone.0107639

    Figure Lengend Snippet: Inhibition of the NLRP3 inflammasome with glyburide (Glyb) prevents caspase-1 activation and IL-1β production by LPS-challenged cardiac fibroblasts (CFs). CFs were pretreated with either vehicle or glyburide (50 µM or 200 µM) 30 min before the LPS (1 µg/ml) challenge. Twenty-four hrs after LPS stimulation, the cells were harvested and processed for the measurement (Western blot) of intracellular NLRP3 (A), pro-caspase-1 (B), activated caspase-1 p10 (C), pro-IL-1β (D), and mature IL-1β (E). The supernatants were harvested for the detection of released IL-1β with ELISA (F). The basal levels of the various components of the NLRP3 inflammasome/IL-1β axis were not affected by glyburide. For A through E, representative blots and densitometric analyses are shown. n = 3 for all experiments (A–F). *p

    Article Snippet: The potential role of IL-1β on cAMP accumulation was studied by adding IL-1β (5 ng/mL) (Millipore, Billerica, MA, USA) to naïve cardiomyocytes as indicated.

    Techniques: Inhibition, Activation Assay, Western Blot, Enzyme-linked Immunosorbent Assay

    Exosome‐delivered mesenchymal‐epithelial transition factor (MET) stimulates macrophages to facilitate tumour growth in vivo. A, The effects of the supernatant from macrophage treated with PBS, MET + exosomes, MET − exosomes, MET − exosomes + recombinant IL‐1β protein, MET + exosomes + IL‐1β neutralizing antibody on tumour growth in a xenograft model. Tumour volume in the xenograft models was measured every 3 d after a 10 d inoculation period. B,C, Final tumour weights were determined and photographed. * P

    Journal: Journal of Cellular and Molecular Medicine

    Article Title: Helicobacter pylori‐induced exosomal MET educates tumour‐associated macrophages to promote gastric cancer progression, et al. Helicobacter pylori‐induced exosomal MET educates tumour‐associated macrophages to promote gastric cancer progression

    doi: 10.1111/jcmm.13847

    Figure Lengend Snippet: Exosome‐delivered mesenchymal‐epithelial transition factor (MET) stimulates macrophages to facilitate tumour growth in vivo. A, The effects of the supernatant from macrophage treated with PBS, MET + exosomes, MET − exosomes, MET − exosomes + recombinant IL‐1β protein, MET + exosomes + IL‐1β neutralizing antibody on tumour growth in a xenograft model. Tumour volume in the xenograft models was measured every 3 d after a 10 d inoculation period. B,C, Final tumour weights were determined and photographed. * P

    Article Snippet: MGC‐803 cells were incubated in the supernatant of THP‐1‐derived macrophages, which were stimulated with PBS, MET+ exosomes, MET− exosomes, MET− exosomes + IL‐1β (PeproTech, Rocky Hill, NJ, USA, #AF‐200‐01B, 1 ng/mL), or MET+ exosomes + IL‐1β neutralizing antibody (Abcam, #ab9722, 3 μg/mL).

    Techniques: In Vivo, Recombinant

    Effects of HG on the secretion of IL-1β and IL-18 in HPMCs. HPMCs were treated with 76, 126 and 214 mM glucose for 6, 12, 24 and 48 h. The levels of (A) IL-18 and (B) IL-1β in the supernatant were detected using enzyme-linked immunosorbent

    Journal: Molecular Medicine Reports

    Article Title: Zinc inhibits high glucose-induced NLRP3 inflammasome activation in human peritoneal mesothelial cells

    doi: 10.3892/mmr.2017.7236

    Figure Lengend Snippet: Effects of HG on the secretion of IL-1β and IL-18 in HPMCs. HPMCs were treated with 76, 126 and 214 mM glucose for 6, 12, 24 and 48 h. The levels of (A) IL-18 and (B) IL-1β in the supernatant were detected using enzyme-linked immunosorbent

    Article Snippet: Each membrane was incubated at 4°C overnight with primary antibodies against NLRP3 (cat. no. ab214185; Abcam, Cambridge, MA, USA; 1:1,000 dilution), Pro-caspase-1 (cat. no. ab14367; Abcam; 1:1,000 dilution), Caspase-1 (cat. no. #4199; Cell Signaling Technology, Inc.; 1:1,000 dilution), HO-1 (cat. no. #5853; Cell Signaling Technology, Inc.; 1:1,000 dilution), NQO1 (cat. no. #3187; Cell Signaling Technology, Inc.; 1:1,000 dilution), IL-1β (cat. no. MAB601; R & D Systems, Inc., Minneapolis, MN, USA; 1:500 dilution), IL-18 (cat. no. D043-3; R & D Systems, Inc.; 1:1,000 dilution) and b-actin (cat. no. #3700; Cell Signaling Technology, Inc.; 1:1,000 dilution) as a control.

    Techniques:

    Effects of Zn intervention on HG-induced levels of IL-1β and IL-18 in HPMCs. The HPMCs were pretreated with 10 µM ZnSO 4 or 1 µM TPEN for 24 h and then incubated with 126 mM glucose for 24 h. The levels of (A) IL-1β and

    Journal: Molecular Medicine Reports

    Article Title: Zinc inhibits high glucose-induced NLRP3 inflammasome activation in human peritoneal mesothelial cells

    doi: 10.3892/mmr.2017.7236

    Figure Lengend Snippet: Effects of Zn intervention on HG-induced levels of IL-1β and IL-18 in HPMCs. The HPMCs were pretreated with 10 µM ZnSO 4 or 1 µM TPEN for 24 h and then incubated with 126 mM glucose for 24 h. The levels of (A) IL-1β and

    Article Snippet: Each membrane was incubated at 4°C overnight with primary antibodies against NLRP3 (cat. no. ab214185; Abcam, Cambridge, MA, USA; 1:1,000 dilution), Pro-caspase-1 (cat. no. ab14367; Abcam; 1:1,000 dilution), Caspase-1 (cat. no. #4199; Cell Signaling Technology, Inc.; 1:1,000 dilution), HO-1 (cat. no. #5853; Cell Signaling Technology, Inc.; 1:1,000 dilution), NQO1 (cat. no. #3187; Cell Signaling Technology, Inc.; 1:1,000 dilution), IL-1β (cat. no. MAB601; R & D Systems, Inc., Minneapolis, MN, USA; 1:500 dilution), IL-18 (cat. no. D043-3; R & D Systems, Inc.; 1:1,000 dilution) and b-actin (cat. no. #3700; Cell Signaling Technology, Inc.; 1:1,000 dilution) as a control.

    Techniques: Incubation

    Recombinant human interleukin-1 receptor antagonist (RhIL-1Ra) ameliorated ConA-induced NOD-like receptor protein 3 (NLRP3) inflammasome activation and pyroptosis. (A) BALB/c mice ( n = 6 for each group) were pretreated with rhIL-1Ra before ConA injection, and samples were extracted at 12 h post ConA treatment. Serum IL-1β and IL-18 were detected by ELISA. (B) Liver homogenates were subjected to caspase-1 activity assay. (C) Western blot of NLRP3, Cleaved caspase-1, and IL-1β in the livers. GAPDH acted as a loading control. Each lane represented a separate animal. Results were obtained from three experiments. Quantification of protein expression were obtained by Image J software. (D) Caspase-1 positive death cells staining were observed by confocal microscopy. FAM-YVAD-FMK (green), propidium iodide (red), Hoechst 33342 (blue). The data were presented as means ± SD (Student’s t -test, * p

    Journal: Frontiers in Immunology

    Article Title: NOD-Like Receptor Protein 3 Inflammasome-Dependent IL-1β Accelerated ConA-Induced Hepatitis

    doi: 10.3389/fimmu.2018.00758

    Figure Lengend Snippet: Recombinant human interleukin-1 receptor antagonist (RhIL-1Ra) ameliorated ConA-induced NOD-like receptor protein 3 (NLRP3) inflammasome activation and pyroptosis. (A) BALB/c mice ( n = 6 for each group) were pretreated with rhIL-1Ra before ConA injection, and samples were extracted at 12 h post ConA treatment. Serum IL-1β and IL-18 were detected by ELISA. (B) Liver homogenates were subjected to caspase-1 activity assay. (C) Western blot of NLRP3, Cleaved caspase-1, and IL-1β in the livers. GAPDH acted as a loading control. Each lane represented a separate animal. Results were obtained from three experiments. Quantification of protein expression were obtained by Image J software. (D) Caspase-1 positive death cells staining were observed by confocal microscopy. FAM-YVAD-FMK (green), propidium iodide (red), Hoechst 33342 (blue). The data were presented as means ± SD (Student’s t -test, * p

    Article Snippet: The primary antibodies used for western blot, including antibodies to NLRP3 (15101), Cleaved caspase-1 (67314), IL-1β (12242), GAPDH (51332), JAK2 (3230), p-JAK2 (Tyr1007/1008) (3776), STAT3 (4904), and p-STAT3 (Tyr705) (91315), were purchased from Cell Signaling Technology (Danvers, MA, USA).

    Techniques: Recombinant, Activation Assay, Mouse Assay, Injection, Enzyme-linked Immunosorbent Assay, Activity Assay, Western Blot, Expressing, Software, Staining, Confocal Microscopy

    Administration of ConA-induced inflammatory cells infiltration into liver tissues followed by reactive oxygen species (ROS) generation. ROS contributed to NOD-like receptor protein 3 inflammasome activation and caspase-1 cleavage, which elicited IL-1β production and pyroptosis, thus accelerating liver inflammation and injury.

    Journal: Frontiers in Immunology

    Article Title: NOD-Like Receptor Protein 3 Inflammasome-Dependent IL-1β Accelerated ConA-Induced Hepatitis

    doi: 10.3389/fimmu.2018.00758

    Figure Lengend Snippet: Administration of ConA-induced inflammatory cells infiltration into liver tissues followed by reactive oxygen species (ROS) generation. ROS contributed to NOD-like receptor protein 3 inflammasome activation and caspase-1 cleavage, which elicited IL-1β production and pyroptosis, thus accelerating liver inflammation and injury.

    Article Snippet: The primary antibodies used for western blot, including antibodies to NLRP3 (15101), Cleaved caspase-1 (67314), IL-1β (12242), GAPDH (51332), JAK2 (3230), p-JAK2 (Tyr1007/1008) (3776), STAT3 (4904), and p-STAT3 (Tyr705) (91315), were purchased from Cell Signaling Technology (Danvers, MA, USA).

    Techniques: Activation Assay

    N -acetyl-cysteine (NAC) attenuated ConA-induced hepatitis via suppressing NOD-like receptor protein 3 (NLRP3) inflammasome activation. (A) BALB/c mice ( n = 6 for each group) were pretreated with NAC and subsequent exposed to ConA challenge for 12 h, then sacrificed for collecting samples. Representative hematoxylin and eosin images of liver tissues were shown (100×, magnification: 400×). (B) Serum ALT and aspartate transaminase (AST) activity were assessed. (C) Western blot was performed to detect NLRP3 inflammasome-associated protein NLRP3, Cleaved caspase-1 and IL-1β in the livers. Each lane represented a separate animal. Results shown represented three independent experiments. Quantification of protein expression with Image J software. (D) The concentrations of IL-1β and IL-18 in serum were measured by ELISA. (E) Caspase-1 enzymatic activity in liver homogenates. The data were presented as means ± SD (Student’s t -test, * p

    Journal: Frontiers in Immunology

    Article Title: NOD-Like Receptor Protein 3 Inflammasome-Dependent IL-1β Accelerated ConA-Induced Hepatitis

    doi: 10.3389/fimmu.2018.00758

    Figure Lengend Snippet: N -acetyl-cysteine (NAC) attenuated ConA-induced hepatitis via suppressing NOD-like receptor protein 3 (NLRP3) inflammasome activation. (A) BALB/c mice ( n = 6 for each group) were pretreated with NAC and subsequent exposed to ConA challenge for 12 h, then sacrificed for collecting samples. Representative hematoxylin and eosin images of liver tissues were shown (100×, magnification: 400×). (B) Serum ALT and aspartate transaminase (AST) activity were assessed. (C) Western blot was performed to detect NLRP3 inflammasome-associated protein NLRP3, Cleaved caspase-1 and IL-1β in the livers. Each lane represented a separate animal. Results shown represented three independent experiments. Quantification of protein expression with Image J software. (D) The concentrations of IL-1β and IL-18 in serum were measured by ELISA. (E) Caspase-1 enzymatic activity in liver homogenates. The data were presented as means ± SD (Student’s t -test, * p

    Article Snippet: The primary antibodies used for western blot, including antibodies to NLRP3 (15101), Cleaved caspase-1 (67314), IL-1β (12242), GAPDH (51332), JAK2 (3230), p-JAK2 (Tyr1007/1008) (3776), STAT3 (4904), and p-STAT3 (Tyr705) (91315), were purchased from Cell Signaling Technology (Danvers, MA, USA).

    Techniques: Activation Assay, Mouse Assay, AST Assay, Activity Assay, Western Blot, Expressing, Software, Enzyme-linked Immunosorbent Assay

    NOD-like receptor protein 3 (NLRP3) deficiency alleviated ConA-induced liver injury. (A) NLRP3 −/− mice and WT mice ( n = 6 for each group) were treated with ConA (20 mg/kg), and corresponding samples were isolated from mice at 0 and 12 h post ConA challenge. Hepatocellular damage was detected by hematoxylin and eosin (H E) and representative images of liver tissues were shown (100×, magnification: 400×). (B) Serum ALT and aspartate transaminase levels in WT and mice were detected. (C) The protein levels of NLRP3, cleaved caspase-1 and IL-1β in the livers of mice with autoimmune hepatitis (AIH) were analyzed by western blot. GAPDH was used as a loading control. Each lane represented a separate animal. Results shown were obtained from three experiments. Quantification was presented in bar graphs. (D) Pyroptosis was detected by serum lactate dehydrogenase (LDH). (E) Representative fluorescence images of liver tissues co-stained with FAM-YVAD-FMK and propidium iodide (PI). FAM-YVAD-FMK (green), PI (red), Hoechst 33342 (blue). The data were presented as means ± SD (Student’s t -test, * p

    Journal: Frontiers in Immunology

    Article Title: NOD-Like Receptor Protein 3 Inflammasome-Dependent IL-1β Accelerated ConA-Induced Hepatitis

    doi: 10.3389/fimmu.2018.00758

    Figure Lengend Snippet: NOD-like receptor protein 3 (NLRP3) deficiency alleviated ConA-induced liver injury. (A) NLRP3 −/− mice and WT mice ( n = 6 for each group) were treated with ConA (20 mg/kg), and corresponding samples were isolated from mice at 0 and 12 h post ConA challenge. Hepatocellular damage was detected by hematoxylin and eosin (H E) and representative images of liver tissues were shown (100×, magnification: 400×). (B) Serum ALT and aspartate transaminase levels in WT and mice were detected. (C) The protein levels of NLRP3, cleaved caspase-1 and IL-1β in the livers of mice with autoimmune hepatitis (AIH) were analyzed by western blot. GAPDH was used as a loading control. Each lane represented a separate animal. Results shown were obtained from three experiments. Quantification was presented in bar graphs. (D) Pyroptosis was detected by serum lactate dehydrogenase (LDH). (E) Representative fluorescence images of liver tissues co-stained with FAM-YVAD-FMK and propidium iodide (PI). FAM-YVAD-FMK (green), PI (red), Hoechst 33342 (blue). The data were presented as means ± SD (Student’s t -test, * p

    Article Snippet: The primary antibodies used for western blot, including antibodies to NLRP3 (15101), Cleaved caspase-1 (67314), IL-1β (12242), GAPDH (51332), JAK2 (3230), p-JAK2 (Tyr1007/1008) (3776), STAT3 (4904), and p-STAT3 (Tyr705) (91315), were purchased from Cell Signaling Technology (Danvers, MA, USA).

    Techniques: Mouse Assay, Isolation, Western Blot, Fluorescence, Staining

    Caspase-1 deficiency suppressed ConA-induced hepatitis. (A) Caspase-1 −/− mice and WT mice ( n = 6 for each group) were subjected to ConA (20 mg/kg) treatment, and samples were collected after exposure to ConA for 12 h. Representative hematoxylin and eosin images of liver tissues were shown (100×, magnification: 400×). (B) Serum ALT and aspartate transaminase (AST) levels were analyzed. (C) Western blot analysis of NOD-like receptor protein 3, Cleaved caspase-1 and IL-1β in the livers. Densitometric quantification were normalized to GAPDH. Each lane represented a separate animal. Data shown represented three independent experiments. (D) Lactate dehydrogenase (LDH) release into serum was measured as signs of pyroptosis. (E) Pyroptosis in the livers was observed by confocal fluorescence microscopy. FAM-YVAD-FMK (green), propidium iodide (red), Hoechst 33342 (blue). The data were presented as means ± SD (Student’s t -test, * p

    Journal: Frontiers in Immunology

    Article Title: NOD-Like Receptor Protein 3 Inflammasome-Dependent IL-1β Accelerated ConA-Induced Hepatitis

    doi: 10.3389/fimmu.2018.00758

    Figure Lengend Snippet: Caspase-1 deficiency suppressed ConA-induced hepatitis. (A) Caspase-1 −/− mice and WT mice ( n = 6 for each group) were subjected to ConA (20 mg/kg) treatment, and samples were collected after exposure to ConA for 12 h. Representative hematoxylin and eosin images of liver tissues were shown (100×, magnification: 400×). (B) Serum ALT and aspartate transaminase (AST) levels were analyzed. (C) Western blot analysis of NOD-like receptor protein 3, Cleaved caspase-1 and IL-1β in the livers. Densitometric quantification were normalized to GAPDH. Each lane represented a separate animal. Data shown represented three independent experiments. (D) Lactate dehydrogenase (LDH) release into serum was measured as signs of pyroptosis. (E) Pyroptosis in the livers was observed by confocal fluorescence microscopy. FAM-YVAD-FMK (green), propidium iodide (red), Hoechst 33342 (blue). The data were presented as means ± SD (Student’s t -test, * p

    Article Snippet: The primary antibodies used for western blot, including antibodies to NLRP3 (15101), Cleaved caspase-1 (67314), IL-1β (12242), GAPDH (51332), JAK2 (3230), p-JAK2 (Tyr1007/1008) (3776), STAT3 (4904), and p-STAT3 (Tyr705) (91315), were purchased from Cell Signaling Technology (Danvers, MA, USA).

    Techniques: Mouse Assay, AST Assay, Western Blot, Fluorescence, Microscopy

    Blocking IL-1β protected ConA-treated mice from acute hepatitis. (A) BALB/c mice ( n = 6 for each group) were pretreated with recombinant human interleukin-1 receptor antagonist (rhIL-1Ra) and subsequently exposed to ConA challenge for 12 h, then sacrificed for collecting samples. Representative H E images of liver tissues were shown (100×, magnification: 400×). (B) Serum ALT and aspartate transaminase (AST) activity were assessed. (C) Serum TNF-α was analyzed by enzyme-linked immune sorbent assay (ELISA). (D) Representative immunohistochemical images of CD68 or CD11b staining in the liver tissue of mice. Quantification of the number of CD11b-positive cells and CD68-positive cells were obtained in four visual fields (×100) in each group. (E) Level of IL-17 in the serum and livers were assessed by ELISA. (F) Primary splenocytes were treated with 10 µg/ml rhIL-1Ra in the presence of 1 µg/ml ConA. The concentration of IL-17 in the supernatants was measured by ELISA. (G) Western blot was performed to detect JAK2, p-JAK2 (Tyr1007/1008), STAT3, and p-STAT3 (Tyr705) in the livers. Each lane represented a separate animal. The blots were representative of three experiments. Quantification of protein expression with Image J software. The data were presented as means ± SD (Student’s t -test, * p

    Journal: Frontiers in Immunology

    Article Title: NOD-Like Receptor Protein 3 Inflammasome-Dependent IL-1β Accelerated ConA-Induced Hepatitis

    doi: 10.3389/fimmu.2018.00758

    Figure Lengend Snippet: Blocking IL-1β protected ConA-treated mice from acute hepatitis. (A) BALB/c mice ( n = 6 for each group) were pretreated with recombinant human interleukin-1 receptor antagonist (rhIL-1Ra) and subsequently exposed to ConA challenge for 12 h, then sacrificed for collecting samples. Representative H E images of liver tissues were shown (100×, magnification: 400×). (B) Serum ALT and aspartate transaminase (AST) activity were assessed. (C) Serum TNF-α was analyzed by enzyme-linked immune sorbent assay (ELISA). (D) Representative immunohistochemical images of CD68 or CD11b staining in the liver tissue of mice. Quantification of the number of CD11b-positive cells and CD68-positive cells were obtained in four visual fields (×100) in each group. (E) Level of IL-17 in the serum and livers were assessed by ELISA. (F) Primary splenocytes were treated with 10 µg/ml rhIL-1Ra in the presence of 1 µg/ml ConA. The concentration of IL-17 in the supernatants was measured by ELISA. (G) Western blot was performed to detect JAK2, p-JAK2 (Tyr1007/1008), STAT3, and p-STAT3 (Tyr705) in the livers. Each lane represented a separate animal. The blots were representative of three experiments. Quantification of protein expression with Image J software. The data were presented as means ± SD (Student’s t -test, * p

    Article Snippet: The primary antibodies used for western blot, including antibodies to NLRP3 (15101), Cleaved caspase-1 (67314), IL-1β (12242), GAPDH (51332), JAK2 (3230), p-JAK2 (Tyr1007/1008) (3776), STAT3 (4904), and p-STAT3 (Tyr705) (91315), were purchased from Cell Signaling Technology (Danvers, MA, USA).

    Techniques: Blocking Assay, Mouse Assay, Recombinant, AST Assay, Activity Assay, Enzyme-linked Immunosorbent Assay, Immunohistochemistry, Staining, Concentration Assay, Western Blot, Expressing, Software

    NOD-like receptor protein 3 (NLRP3) inflammasome activation and IL-1β production in ConA-induced hepatitis. (A) BALB/c mice ( n = 6 for each group) were intravenous administrated with ConA (20 mg/kg), and sera and liver tissues were obtained following ConA injection at 0, 3, 6, and 12 h. The expression of NLRP3, Cleaved caspase-1, and IL-1β in the livers were detected by western blot analysis. GAPDH was provided as a loading control. Each lane represented a separate animal. The blots were representative of three experiments. Densitometric values of these proteins were quantified using the Image J software. (B) Serum concentrations of IL-1β and IL-18 were analyzed by enzyme-linked immune sorbent assay. (C) Caspase-1 enzymatic activity in the liver homogenates was measured. (D) Lactate dehydrogenase (LDH) release into serum. (E) FAM-YVAD-FMK and propidium iodide (PI) double staining of liver tissues were applied to detect pyroptosis. FAM-YVAD-FMK (green), PI (red), Hoechst 33342 (blue), Scale bars = 50 µm. (F) The protein levels of NLRP3 pathways in the primary hepatocytes and nonparenchymal liver cells isolated from ConA-treated mice were detected by western blot analysis. GAPDH was used as a loading control. Each lane represented a separate animal. Results represented three independent experiments. Quantification was presented. (G) The expression of NLRP3 in primary hepatocytes was displayed by immunofluorescence. NLRP3 (Red), Hoechst 33342 (blue), scale bars = 10 µm. The data were presented as means ± SD (Student’s t -test, * p

    Journal: Frontiers in Immunology

    Article Title: NOD-Like Receptor Protein 3 Inflammasome-Dependent IL-1β Accelerated ConA-Induced Hepatitis

    doi: 10.3389/fimmu.2018.00758

    Figure Lengend Snippet: NOD-like receptor protein 3 (NLRP3) inflammasome activation and IL-1β production in ConA-induced hepatitis. (A) BALB/c mice ( n = 6 for each group) were intravenous administrated with ConA (20 mg/kg), and sera and liver tissues were obtained following ConA injection at 0, 3, 6, and 12 h. The expression of NLRP3, Cleaved caspase-1, and IL-1β in the livers were detected by western blot analysis. GAPDH was provided as a loading control. Each lane represented a separate animal. The blots were representative of three experiments. Densitometric values of these proteins were quantified using the Image J software. (B) Serum concentrations of IL-1β and IL-18 were analyzed by enzyme-linked immune sorbent assay. (C) Caspase-1 enzymatic activity in the liver homogenates was measured. (D) Lactate dehydrogenase (LDH) release into serum. (E) FAM-YVAD-FMK and propidium iodide (PI) double staining of liver tissues were applied to detect pyroptosis. FAM-YVAD-FMK (green), PI (red), Hoechst 33342 (blue), Scale bars = 50 µm. (F) The protein levels of NLRP3 pathways in the primary hepatocytes and nonparenchymal liver cells isolated from ConA-treated mice were detected by western blot analysis. GAPDH was used as a loading control. Each lane represented a separate animal. Results represented three independent experiments. Quantification was presented. (G) The expression of NLRP3 in primary hepatocytes was displayed by immunofluorescence. NLRP3 (Red), Hoechst 33342 (blue), scale bars = 10 µm. The data were presented as means ± SD (Student’s t -test, * p

    Article Snippet: The primary antibodies used for western blot, including antibodies to NLRP3 (15101), Cleaved caspase-1 (67314), IL-1β (12242), GAPDH (51332), JAK2 (3230), p-JAK2 (Tyr1007/1008) (3776), STAT3 (4904), and p-STAT3 (Tyr705) (91315), were purchased from Cell Signaling Technology (Danvers, MA, USA).

    Techniques: Activation Assay, Mouse Assay, Injection, Expressing, Western Blot, Software, Activity Assay, Double Staining, Isolation, Immunofluorescence