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il 25 (R&D Systems)

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Transcriptional regulation of SLC40A1 by TGF-β1. a HPFs were treated for 48 h with different cytokines [TGF-β1 (5 ng/ml), WNT-1(50 ng/ml), WNT-3a (50 ng/ml), WNT-5a (50 ng/ml), TNFα (10 ng/ml), LPS (1,000 ng/ml), IL-1β (10 ng/ml), IL-4 (20 ng/ml), IL-5 (20 ng/ml), IL-13 (25 ng/ml), IL-21 (25 <t>ng/ml),</t> <t>IL-25</t> (25 ng/ml), IL-33 (30 ng/ml), IFNβ (1 ng/mL), or IFNγ (20 ng/ml)]. SLC40A1 mRNA levels were determined by real-time PCR and expressed a ratio of the control (CON). b HPFs were treated with 50 ng/ml IL-6 for 48 h or serum-starved for 4 h or 24 h and then treated with 10 nM thrombin or 100 nM factor Xa for 48 h and SLC40A1 mRNA levels were determined by real-time PCR. c HPFs were co-transfected with the pGL3-Basic vector containing the SLC40A1 promoter fragment and firefly luciferase gene (180 ng) along with pRL-TK plasmid containing Renilla luciferase gene (20 ng) and then treated with 5 ng/ml TGF-β1 for 48 h. Firefly and Renilla luciferase activities in cell lysates were measured. The relative firefly luciferase activities were normalized to the respective Renilla luciferase activities. The results are presented as a ratio CON. d HPFs were treated with shSMAD2, shSMAD3, or shCON lentivirus at a MOI of 100 for 48 h. SMAD2 and SMAD3 protein levels were determined by western blot and quantitated. e HPFs were treated with shSMAD2, shSMAD3, or shCON lentivirus at a MOI of 100 for 48 h and then treated with 5 ng/ml TGF-β1 for 48 h. SLC40A1 mRNA levels were determined by real-time PCR. f HPFs were treated with SIS3 (10 µM, Milipore Sigma, Cat# 566405) for 2 h and then with TGF-β1 (5 ng/ml) for 48 h. SLC40A1 mRNA levels were determined by real-time PCR. g HPFs were treated with TGF-β1 (5 ng/ml) for 48 h. The cell lysates were subjected to chromatin immunoprecipitation (ChIP) using anti-SMAD3 antibodies. The SMAD3 binding site on the SLC40A1 promoter was detected by real-time PCR. n =3, * p < 0.05, ** p < 0.01, *** p < 0.001 v.s CON or shCON. ## p < 0.01 vs ShCon/TGF-β1. Student t-test ( c ), one-way ANOVA ( a and d ) or two-way ANOVA ( b , e , f and g ). followed by uncorrected Fisher’s least significant difference (LSD) test ( e , f and g ) or Turkey’s multiple comparison test ( b )

Il 25, supplied by R&D Systems, used in various techniques. Bioz Stars score: 94/100, based on 18 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/recombinant+human+il+25/Recombinant+Human+IL-17E+Protein/pmc12922364-90-70-74
Average 94 stars, based on 18 article reviews

il 25 - by Bioz Stars, 2026-10

94/100 stars

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1) Product Images from "Downregulation of SLC40A1 leads to iron accumulation in fibrotic lung fibroblasts"

Article Title: Downregulation of SLC40A1 leads to iron accumulation in fibrotic lung fibroblasts

Journal: Respiratory Research

doi: 10.1186/s12931-025-03479-0

Figure Legend Snippet: Transcriptional regulation of SLC40A1 by TGF-β1. a HPFs were treated for 48 h with different cytokines [TGF-β1 (5 ng/ml), WNT-1(50 ng/ml), WNT-3a (50 ng/ml), WNT-5a (50 ng/ml), TNFα (10 ng/ml), LPS (1,000 ng/ml), IL-1β (10 ng/ml), IL-4 (20 ng/ml), IL-5 (20 ng/ml), IL-13 (25 ng/ml), IL-21 (25 ng/ml), IL-25 (25 ng/ml), IL-33 (30 ng/ml), IFNβ (1 ng/mL), or IFNγ (20 ng/ml)]. SLC40A1 mRNA levels were determined by real-time PCR and expressed a ratio of the control (CON). b HPFs were treated with 50 ng/ml IL-6 for 48 h or serum-starved for 4 h or 24 h and then treated with 10 nM thrombin or 100 nM factor Xa for 48 h and SLC40A1 mRNA levels were determined by real-time PCR. c HPFs were co-transfected with the pGL3-Basic vector containing the SLC40A1 promoter fragment and firefly luciferase gene (180 ng) along with pRL-TK plasmid containing Renilla luciferase gene (20 ng) and then treated with 5 ng/ml TGF-β1 for 48 h. Firefly and Renilla luciferase activities in cell lysates were measured. The relative firefly luciferase activities were normalized to the respective Renilla luciferase activities. The results are presented as a ratio CON. d HPFs were treated with shSMAD2, shSMAD3, or shCON lentivirus at a MOI of 100 for 48 h. SMAD2 and SMAD3 protein levels were determined by western blot and quantitated. e HPFs were treated with shSMAD2, shSMAD3, or shCON lentivirus at a MOI of 100 for 48 h and then treated with 5 ng/ml TGF-β1 for 48 h. SLC40A1 mRNA levels were determined by real-time PCR. f HPFs were treated with SIS3 (10 µM, Milipore Sigma, Cat# 566405) for 2 h and then with TGF-β1 (5 ng/ml) for 48 h. SLC40A1 mRNA levels were determined by real-time PCR. g HPFs were treated with TGF-β1 (5 ng/ml) for 48 h. The cell lysates were subjected to chromatin immunoprecipitation (ChIP) using anti-SMAD3 antibodies. The SMAD3 binding site on the SLC40A1 promoter was detected by real-time PCR. n =3, * p < 0.05, ** p < 0.01, *** p < 0.001 v.s CON or shCON. ## p < 0.01 vs ShCon/TGF-β1. Student t-test ( c ), one-way ANOVA ( a and d ) or two-way ANOVA ( b , e , f and g ). followed by uncorrected Fisher’s least significant difference (LSD) test ( e , f and g ) or Turkey’s multiple comparison test ( b )

Techniques Used: Real-time Polymerase Chain Reaction, Control, Transfection, Plasmid Preparation, Luciferase, Western Blot, Chromatin Immunoprecipitation, Binding Assay, Comparison

Single Cell:

Article Title: Identification of functional roles for both IL-17RB and IL-17RA in mediating IL-25-induced activities.
Article Snippet: PBMC were isolated from heparinized human whole blood obtained from normal donors and set up in culture at 5 106 cells/ml for 24 h with 100 ng/ml recombinant human thymic stromal lymphopoietin (TSLP; Amgen) in X-VIVO 15 (Lonza) plus 5% human AB serum (Lonza). .. PBMC were then collected and set up in restimulation cultures as single-cell suspensions at 4 106 cells/well in 48-well plates with 0.5-ml final volume/well in the presence of 10 ng/ml recombinant human IL-2 (R&D Systems), 10 ng/ml recombinant human IL-25 (R&D Systems), or various concentrations of recombinant human IL-17A (R&D Systems). .. Inhibition experiments were performed in the presence or absence of 10 g/ml soluble human IL-17RB.Fc (R&D Systems), 10 g/ml goat anti-human IL-17RA Ab (R&D Systems; catalog no. AF177), 10 g/ml mouse anti-human IL17RA mAb clone 133621 (R&D Systems; catalog no. MAB1771), 10 g/ml soluble human IL-17RA.Fc (Amgen) (20), 10 g/ml mouse antihuman IL-17A mAb clone 41809 (R&D Systems; catalog no. MAB317), or 10 g/ml of an appropriate protein control.

Recombinant:

Article Title: Interleukin-25-Mediated-IL-17RB Upregulation Promotes Cutaneous Wound Healing in Diabetic Mice by Improving Endothelial Cell Functions
Article Snippet: .. Recombinant mouse IL-25 (rmIL-25, Cat#: 587306) was brought from Biolegend, recombinant human IL-25 (rhIL-25, Cat#: 8134-IL) was purchased from R&D systems and prepared following instructions. .. Rabbit anti-CD31 antibody (Cat#: GB11063-2) was obtained from Servicebio.

Article Title: IL-25 drives remodelling in allergic airways disease induced by house dust mite
Article Snippet: .. Normal human lung fibroblasts (NHLFs; Lonza, Basel, Switzerland) were cultured in six well plates in functionally graded materials supplemented with 10% FCS/hygromycin B 15 μg/ml in the presence or absence of 20 ng/ml recombinant human IL-25 (R&D systems). ..

Article Title: IL-25 in atopic dermatitis: a possible link between inflammation and skin barrier dysfunction?
Article Snippet: .. For the analysis of filaggrin mRNA level, cells were stimulated at 70–80% confluency with carrier-free recombinant human IL-25 (10 and 20 ng ml 1) (1258-IL; R&D Systems) for 5 days. ..

Article Title: Interleukin-25 Produced by Synoviocytes Has Anti-inflammatory Effects by Acting As a Receptor Antagonist for Interleukin-17A Function
Article Snippet: Cells were cultured at 37°C/5% CO 2 in DMEM medium (Eurobio, Courtaboeuf, France) supplemented with 10% fetal bovine serum (Life Technologies, Carlsbad, CA, USA), 2% penicillin–streptomycin (Eurobio, Courtaboeuf, France), 1% l -glutamine (Eurobio, Courtaboeuf, France), and 1% amphotericin B (Eurobio, Courtaboeuf, France). .. For cytokine treatments, cells were plated at a density of 5 × 10 4 cells/cm 2 and left for adhesion overnight before the addition of 50 ng/mL recombinant human IL-17A, 0.5 ng/mL recombinant human TNF-α and/or 50 ng/mL recombinant human IL-25 (all from R&D Systems, Minneapolis, MN, USA). .. For IL-25 blocking experiments, synoviocyte supernatants from late time points were incubated for 1 h at 37°C in the presence of an anti-IL-25 polyclonal antibody 10 μg/mL or of a polyclonal goat control IgG (all from R&D Systems, Minneapolis, MN, USA) at 10 μg/mL.

Cell Culture:

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Journal: Respiratory Research

Article Title: Downregulation of SLC40A1 leads to iron accumulation in fibrotic lung fibroblasts

doi: 10.1186/s12931-025-03479-0

Figure Lengend Snippet: Transcriptional regulation of SLC40A1 by TGF-β1. a HPFs were treated for 48 h with different cytokines [TGF-β1 (5 ng/ml), WNT-1(50 ng/ml), WNT-3a (50 ng/ml), WNT-5a (50 ng/ml), TNFα (10 ng/ml), LPS (1,000 ng/ml), IL-1β (10 ng/ml), IL-4 (20 ng/ml), IL-5 (20 ng/ml), IL-13 (25 ng/ml), IL-21 (25 ng/ml), IL-25 (25 ng/ml), IL-33 (30 ng/ml), IFNβ (1 ng/mL), or IFNγ (20 ng/ml)]. SLC40A1 mRNA levels were determined by real-time PCR and expressed a ratio of the control (CON). b HPFs were treated with 50 ng/ml IL-6 for 48 h or serum-starved for 4 h or 24 h and then treated with 10 nM thrombin or 100 nM factor Xa for 48 h and SLC40A1 mRNA levels were determined by real-time PCR. c HPFs were co-transfected with the pGL3-Basic vector containing the SLC40A1 promoter fragment and firefly luciferase gene (180 ng) along with pRL-TK plasmid containing Renilla luciferase gene (20 ng) and then treated with 5 ng/ml TGF-β1 for 48 h. Firefly and Renilla luciferase activities in cell lysates were measured. The relative firefly luciferase activities were normalized to the respective Renilla luciferase activities. The results are presented as a ratio CON. d HPFs were treated with shSMAD2, shSMAD3, or shCON lentivirus at a MOI of 100 for 48 h. SMAD2 and SMAD3 protein levels were determined by western blot and quantitated. e HPFs were treated with shSMAD2, shSMAD3, or shCON lentivirus at a MOI of 100 for 48 h and then treated with 5 ng/ml TGF-β1 for 48 h. SLC40A1 mRNA levels were determined by real-time PCR. f HPFs were treated with SIS3 (10 µM, Milipore Sigma, Cat# 566405) for 2 h and then with TGF-β1 (5 ng/ml) for 48 h. SLC40A1 mRNA levels were determined by real-time PCR. g HPFs were treated with TGF-β1 (5 ng/ml) for 48 h. The cell lysates were subjected to chromatin immunoprecipitation (ChIP) using anti-SMAD3 antibodies. The SMAD3 binding site on the SLC40A1 promoter was detected by real-time PCR. n =3, * p < 0.05, ** p < 0.01, *** p < 0.001 v.s CON or shCON. ## p < 0.01 vs ShCon/TGF-β1. Student t-test ( c ), one-way ANOVA ( a and d ) or two-way ANOVA ( b , e , f and g ). followed by uncorrected Fisher’s least significant difference (LSD) test ( e , f and g ) or Turkey’s multiple comparison test ( b )

Article Snippet: HPFs (1x10 5 /well) were seeded into 12-well plates and treated with different cytokines and other compounds for 48 h: TNF-α (10 ng/ml, #300-01A, PeproTech, Cranbury, NJ, USA), lipopolysaccharides (LPS) (1,000 ng/ml, #00–4976-93, Invitrogen), TGF-β1 (5 ng/ml, #240-B, R&D Systems, Minneapolis, MN, USA) , IL-4 (20 ng/ml, #200-04, PeproTech), IFN-γ (20 ng/ml, #300-02, PeproTech) , IL-21 (25 ng/ml, #200-21, PeproTech), IL-13 (25 ng/ml, #200-13, PeproTech), IFN-β (1 ng/mL, #300-02BC, PeproTech), IL-25 (25 ng/ml, #1258-IL, R&D Systems), IL-33 (30 ng/ml, #200-33, PeproTech), WNT-1 (50 ng/ml, #120-17, PeproTech), IL-1β (10 ng/ml, #200-01B, PeproTech), IL-5 (20 ng/ml, #200-05, PeproTech), WNT-3a (50 ng/mL, #5036-WN, R&D Systems), WNT-5a (50 g/mL, #645-WN, R&D Systems), IL-6 (50 ng/ml, #200-06, Gibco), thrombin (10 nM, #RP-43100, Invitrogen), factor Xa (100 nM, #RP-43114, Invitrogen), ferric ammonium citrate (FAC) (200 μM, # RES20400 -A7, Sigma), deferoxamine (DFO) (10 μM #D9533, Sigma).

Techniques: Real-time Polymerase Chain Reaction, Control, Transfection, Plasmid Preparation, Luciferase, Western Blot, Chromatin Immunoprecipitation, Binding Assay, Comparison

PD-L1 expression positively correlates with proinflammatory markers in M1-polarized macrophages. (A-C) PD-L1-overexpressing (PD-L1 HI ) and control (PD-L1 NC ) THP-1-M cells were stimulated with LPS (100 ng/ml) + IFN-γ (20 ng/ml) for 12 h followed by RNA sequencing. A Heatmap of inflammatory gene expression in PD-L1 HI vs. PD-L1 NC cells. B MA plot showing differential gene expression between PD-L1 HI and PD-L1 NC cells. C TPM expression values of IL-6, IL-27 and NOS2. D - E PD-L1 HI and PD-L1 NC cells were stimulated with LPS + IFN-γ for 24 h. ( n = 3 independent biological replicates) ( D ) qRT-PCR analysis of IL-6, IL-27 and NOS2 mRNA levels ( n = 3 independent biological replicates). E ELISA for IL-6/IL-27 and Griess reagent assay for NO in supernatants ( n = 3 independent biological replicates). (F-G) PD-L1-knockout THP-1-M (PD-L1 KO /THP-1-M) and PD-L1 NC /THP-1-M were stimulated with LPS + IFN-γ for 24 h. F qRT-PCR analysis of IL-6, IL-27 and NOS2 mRNA levels ( n = 3 independent biological replicates). G ELISA and Griess reagent detection of IL-6/IL-27 proteins and NO in supernatants ( n = 3 independent biological replicates). The data are presented as the mean ± SEM. Statistical analysis for C, D, E, F and G was performed by Student’s t-test. * p < 0.05

Journal: Cell Communication and Signaling : CCS

Article Title: PD-L1 mediates M1 polarization of macrophages via the AIM2/IL-18/STAT1 signaling axis during sepsis

doi: 10.1186/s12964-025-02578-1

Figure Lengend Snippet: PD-L1 expression positively correlates with proinflammatory markers in M1-polarized macrophages. (A-C) PD-L1-overexpressing (PD-L1 HI ) and control (PD-L1 NC ) THP-1-M cells were stimulated with LPS (100 ng/ml) + IFN-γ (20 ng/ml) for 12 h followed by RNA sequencing. A Heatmap of inflammatory gene expression in PD-L1 HI vs. PD-L1 NC cells. B MA plot showing differential gene expression between PD-L1 HI and PD-L1 NC cells. C TPM expression values of IL-6, IL-27 and NOS2. D - E PD-L1 HI and PD-L1 NC cells were stimulated with LPS + IFN-γ for 24 h. ( n = 3 independent biological replicates) ( D ) qRT-PCR analysis of IL-6, IL-27 and NOS2 mRNA levels ( n = 3 independent biological replicates). E ELISA for IL-6/IL-27 and Griess reagent assay for NO in supernatants ( n = 3 independent biological replicates). (F-G) PD-L1-knockout THP-1-M (PD-L1 KO /THP-1-M) and PD-L1 NC /THP-1-M were stimulated with LPS + IFN-γ for 24 h. F qRT-PCR analysis of IL-6, IL-27 and NOS2 mRNA levels ( n = 3 independent biological replicates). G ELISA and Griess reagent detection of IL-6/IL-27 proteins and NO in supernatants ( n = 3 independent biological replicates). The data are presented as the mean ± SEM. Statistical analysis for C, D, E, F and G was performed by Student’s t-test. * p < 0.05

Article Snippet: IL-27, IL-6, IL-18, and IFN-γ concentrations in cell supernatants or plasma were quantified using ELISA kits (Boster Biological Technology; Wuhan, China) with absorbance measurements at 450 nm.

Techniques: Expressing, Control, RNA Sequencing, Gene Expression, Quantitative RT-PCR, Enzyme-linked Immunosorbent Assay, Knock-Out

Triple-verification strategy (gene silencing/antibody neutralization/site-directed mutagenesis) confirms regulatory hierarchy of PD-L1/AIM2/IL-18/STAT1 signaling axis in macrophage M1 polarization. A PD-L1 HI /THP-1-M and PD-L1 NC /THP-1-M cells were pretreated with AIM2-targeting siRNA or scramble siRNA (scr siRNA) prior to 24 h LPS (100 ng/ml) + IFN-γ (20 ng/ml) co-stimulation, with subsequent Western blotting analysis of STAT1 phosphorylation. B - C Anti-IL-18 neutralizing antibody (1 µg/ml) and isotype control (1 µg/ml) were pretreated for 24 h followed by LPS + IFN-γ 24 h co-stimulation. B qRT-PCR quantification of IFN-γ mRNA ( n = 3 independent biological replicates). C STAT1 phosphorylation profiling by Western blotting. D Truncation mutant validation: LPS + IFN-γ-stimulated (24 h) PD-L1 Δ35–90 cells analyzed for STAT1 activation vs. full length type. E Following AIM2 silencing in PD-L1 HI /THP-1-M and PD-L1 NC /THP-1-M cells, qRT-PCR quantification of IL-6, IL-27 and NOS2 mRNA after 24 h LPS + IFN-γ stimulation ( n = 3 independent biological replicates). F Post IL-18 neutralization, mRNA levels of IL-6, IL-27 and NOS2 were assessed by qRT-PCR under LPS + IFN-γ 24 h stimulation ( n = 3 independent biological replicates). G STAT1-silenced cells were analyzed for IL-6/IL-27/NOS2 transcriptional changes post 24 h LPS + IFN-γ exposure ( n = 3 independent biological replicates). H Truncated PD-L1 Δ35–90 mutants were evaluated for IL-6, IL-27 and NOS2 mRNA expression following LPS + IFN-γ 24 h challenge ( n = 3 independent biological replicates). The data are presented as the mean ± SEM. Statistical analysis for B, E, F, G and H was performed by Student’s t-test. * p < 0.05

Journal: Cell Communication and Signaling : CCS

Article Title: PD-L1 mediates M1 polarization of macrophages via the AIM2/IL-18/STAT1 signaling axis during sepsis

doi: 10.1186/s12964-025-02578-1

Figure Lengend Snippet: Triple-verification strategy (gene silencing/antibody neutralization/site-directed mutagenesis) confirms regulatory hierarchy of PD-L1/AIM2/IL-18/STAT1 signaling axis in macrophage M1 polarization. A PD-L1 HI /THP-1-M and PD-L1 NC /THP-1-M cells were pretreated with AIM2-targeting siRNA or scramble siRNA (scr siRNA) prior to 24 h LPS (100 ng/ml) + IFN-γ (20 ng/ml) co-stimulation, with subsequent Western blotting analysis of STAT1 phosphorylation. B - C Anti-IL-18 neutralizing antibody (1 µg/ml) and isotype control (1 µg/ml) were pretreated for 24 h followed by LPS + IFN-γ 24 h co-stimulation. B qRT-PCR quantification of IFN-γ mRNA ( n = 3 independent biological replicates). C STAT1 phosphorylation profiling by Western blotting. D Truncation mutant validation: LPS + IFN-γ-stimulated (24 h) PD-L1 Δ35–90 cells analyzed for STAT1 activation vs. full length type. E Following AIM2 silencing in PD-L1 HI /THP-1-M and PD-L1 NC /THP-1-M cells, qRT-PCR quantification of IL-6, IL-27 and NOS2 mRNA after 24 h LPS + IFN-γ stimulation ( n = 3 independent biological replicates). F Post IL-18 neutralization, mRNA levels of IL-6, IL-27 and NOS2 were assessed by qRT-PCR under LPS + IFN-γ 24 h stimulation ( n = 3 independent biological replicates). G STAT1-silenced cells were analyzed for IL-6/IL-27/NOS2 transcriptional changes post 24 h LPS + IFN-γ exposure ( n = 3 independent biological replicates). H Truncated PD-L1 Δ35–90 mutants were evaluated for IL-6, IL-27 and NOS2 mRNA expression following LPS + IFN-γ 24 h challenge ( n = 3 independent biological replicates). The data are presented as the mean ± SEM. Statistical analysis for B, E, F, G and H was performed by Student’s t-test. * p < 0.05

Techniques: Neutralization, Mutagenesis, Western Blot, Phospho-proteomics, Control, Quantitative RT-PCR, Biomarker Discovery, Activation Assay, Expressing

PD-L1 knockout reduces septic mortality dampens systemic inflammation and alleviates vital organ (cardiac/hepatic/renal) injury in murine models. A PD-L1 wild-type (WT) and knockout (KO) mice were subjected to CLP followed by survival monitoring, inflammatory marker assessment, and multi-organ functional evaluation. B Survival rates of PD-L1 WT and PD-L1 KO mice at indicated time points post-CLP ( n = 15 mice per group). Results were compared by log-rank test. C mRNA levels of IL-6, IL-27, and NOS2 in monocytes analyzed by qRT-PCR at 24 h post-CLP ( n = 3 mice per group). D Serum concentrations of IL-6 and IL-27 proteins measured by ELISA, and NO levels determined by Griess assay at 24 h post-CLP ( n = 3 mice per group). E Serum biomarkers of organ function including ALT and AST for hepatic injury, BUN for renal dysfunction, and cTnI for cardiac damage at 24 h post-CLP ( n = 3 mice per group). The data are presented as the mean ± SEM. Statistical analysis for C, D and E was performed by Student’s t-test. * p < 0.05

Journal: Cell Communication and Signaling : CCS

Article Title: PD-L1 mediates M1 polarization of macrophages via the AIM2/IL-18/STAT1 signaling axis during sepsis

doi: 10.1186/s12964-025-02578-1

Figure Lengend Snippet: PD-L1 knockout reduces septic mortality dampens systemic inflammation and alleviates vital organ (cardiac/hepatic/renal) injury in murine models. A PD-L1 wild-type (WT) and knockout (KO) mice were subjected to CLP followed by survival monitoring, inflammatory marker assessment, and multi-organ functional evaluation. B Survival rates of PD-L1 WT and PD-L1 KO mice at indicated time points post-CLP ( n = 15 mice per group). Results were compared by log-rank test. C mRNA levels of IL-6, IL-27, and NOS2 in monocytes analyzed by qRT-PCR at 24 h post-CLP ( n = 3 mice per group). D Serum concentrations of IL-6 and IL-27 proteins measured by ELISA, and NO levels determined by Griess assay at 24 h post-CLP ( n = 3 mice per group). E Serum biomarkers of organ function including ALT and AST for hepatic injury, BUN for renal dysfunction, and cTnI for cardiac damage at 24 h post-CLP ( n = 3 mice per group). The data are presented as the mean ± SEM. Statistical analysis for C, D and E was performed by Student’s t-test. * p < 0.05

Techniques: Knock-Out, Marker, Functional Assay, Quantitative RT-PCR, Enzyme-linked Immunosorbent Assay, Griess Assay

Review

il 25 (R&D Systems)

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