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nmol l tumor necrosis factor  (R&D Systems)


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    Structured Review

    R&D Systems nmol l tumor necrosis factor
    Nmol L Tumor Necrosis Factor, supplied by R&D Systems, used in various techniques. Bioz Stars score: 97/100, based on 1751 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/tnf+%CE%B1/Recombinant+Human+TNF-alpha+Protein/pmc13054578-103-43-49
    Average 97 stars, based on 1751 article reviews
    nmol l tumor necrosis factor - by Bioz Stars, 2026-10
    97/100 stars

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    Related Articles

    Sandwich ELISA:

    Article Title: Vibrio vulnificus MARTX cytotoxin triggers necroptosis-driven macrophage cell death.
    Article Snippet: .. The concentrations of TNF-α (DY410, R&D Systems, Minneapolis, MN, USA) and secretory HMGB1 (sHMGB1, IT5108, G-Biosciences, St. Louis, MO, USA) were subsequently quantified using the sandwich ELISA kits by following the manufacturer's instructions. .. To visualize the localization of MARTX and lipid rafts in cells, RAW264.7 cells (2 × 106) were seeded in 6-cm dishes and incubated for 12 h. Cells were infected with V. vulnificus ΔvvhA (FJ201) or ΔrtxA1/ ΔvvhA (HL114) at an MOI of 10 and incubated at 37 ◦C for 2 h. Cells were washed with PBS and fixed with 4% paraformaldehyde (SigmaAldrich) for 90 min.

    Concentration Assay:

    Article Title: Cellular-state control using ribozyme-scaffolded miRNA-sensing and CRISPR-mediated actuation.
    Article Snippet: The HEK293 and HCT116 cells were grown in Dulbecco’s modified Eagle’s medium (DMEM, Sigma, D5671) supplemented with 10% Fetal Bovine Serum (FBS, Corning, 35-010-CV), 0.1 mM MEM non-essential amino acids (Life Technologies, 11140–050), 0.045 units/mL of Penicillin and 0.045 units/mL of Streptomycin (Penicillin-Streptomycin liquid, Life Technologies, 15140–122). .. Mesenchymal state transition was induced in HCT116 cells by adding TNF-α (R&D Systems 210-TA) at 20ng/mL concentration. ..

    Negative Control:

    Article Title: The anti-ulcerative potential of Berberine on the rat model of inflammatory bowel disease.
    Article Snippet: resulting bowel inflammation is ascribed to the infiltration of inflammatory cells that provoke ulceration in the mucosal lining of colon, moreover, long-standing UC increases the risk of colorectal cancer and morbidity (Bastaki et al. 2018).. Colon ulceration involves both mucosal and submucosal colonial layers (Malago and Sangu 2015).. UC occurs due to chronic inflammation on smooth muscles and elevated contractile responses in the rectum (Limdi and Vasant 2016), and results in epithelial disruption along with subsequent damaged mucosal permeability, leading to uncontrolled uptake of the antigens and sustained activation of intestinal immune system (Ordas et al. 2012).

    Enzyme-linked Immunosorbent Assay:

    Article Title: The anti-ulcerative potential of Berberine on the rat model of inflammatory bowel disease.
    Article Snippet: resulting bowel inflammation is ascribed to the infiltration of inflammatory cells that provoke ulceration in the mucosal lining of colon, moreover, long-standing UC increases the risk of colorectal cancer and morbidity (Bastaki et al. 2018).. Colon ulceration involves both mucosal and submucosal colonial layers (Malago and Sangu 2015).. UC occurs due to chronic inflammation on smooth muscles and elevated contractile responses in the rectum (Limdi and Vasant 2016), and results in epithelial disruption along with subsequent damaged mucosal permeability, leading to uncontrolled uptake of the antigens and sustained activation of intestinal immune system (Ordas et al. 2012).

    Recombinant:


    Clinical Proteomics:

    Article Title: Impact of infusing the cholesterol precursor mevalonate on the hypocholesterolemia of sepsis and its potential consequences: a paradoxical response.
    Article Snippet: .. After sacrifice, plasma HDL- (DZ129A-K, Diazyme Laboratories) and LDL-cholesterol (DZ128A-K, 168 Diazyme Laboratories), TNF-α (MHSTA50, R&D Systems, Minneapolis, MN, USA), CORT 169 (EIA5186, DRG International Inc., Springfield, NJ, USA) and total bile acid (DZ042A-KY1, Diazyme 170 Laboratories) concentrations were measured with commercially available assays, as per 171 manufacturer’s instructions. ..



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    Image Search Results


    In vivo immunomodulatory effects of different modified surfaces in a DM model. (A) Schematic representation of the animal modeling and experimental treatment workflow. (B, C) hematoxylin and eosin staining of the peri-implant tissues in the femurs of DM rats 1 week after implantation, accompanied by quantitative analysis of the fibrous capsule thickness (scale bar = 100 μm, n = 5). (D–G) Immunofluorescence staining evaluating the polarization state of macrophages surrounding the implants (green: macrophage marker cluster of differentiation (CD) 68; red: M1 marker CD86 and M2 marker CD206; blue: nuclei), along with corresponding quantitative analysis of the fluorescence signals (scale bar = 100 μm, n = 5). (H–K) Immunohistochemical staining assessing the expression of the pro-inflammatory marker tumor necrosis factor-α and the anti-inflammatory marker interleukin-10 in the peri-implant area, with quantitative results of the positive staining areas (scale bar = 100 μm, n = 5). Data are expressed as the mean ± standard deviation, with statistical analysis performed using one-way ANOVA and Tukey's post-hoc test. ∗p < 0.05, ∗∗p < 0.01, and ∗∗∗p < 0.001 indicate statistical significance.

    Journal: Bioactive Materials

    Article Title: Integrated apoptotic extracellular vesicle-recruitment peptide coating reprograms the diabetic bone microenvironment and orchestrates enhanced implant osseointegration

    doi: 10.1016/j.bioactmat.2026.05.059

    Figure Lengend Snippet: In vivo immunomodulatory effects of different modified surfaces in a DM model. (A) Schematic representation of the animal modeling and experimental treatment workflow. (B, C) hematoxylin and eosin staining of the peri-implant tissues in the femurs of DM rats 1 week after implantation, accompanied by quantitative analysis of the fibrous capsule thickness (scale bar = 100 μm, n = 5). (D–G) Immunofluorescence staining evaluating the polarization state of macrophages surrounding the implants (green: macrophage marker cluster of differentiation (CD) 68; red: M1 marker CD86 and M2 marker CD206; blue: nuclei), along with corresponding quantitative analysis of the fluorescence signals (scale bar = 100 μm, n = 5). (H–K) Immunohistochemical staining assessing the expression of the pro-inflammatory marker tumor necrosis factor-α and the anti-inflammatory marker interleukin-10 in the peri-implant area, with quantitative results of the positive staining areas (scale bar = 100 μm, n = 5). Data are expressed as the mean ± standard deviation, with statistical analysis performed using one-way ANOVA and Tukey's post-hoc test. ∗p < 0.05, ∗∗p < 0.01, and ∗∗∗p < 0.001 indicate statistical significance.

    Article Snippet: For IHC analysis, sections underwent heat-induced antigen retrieval and blocking prior to incubation with antibodies against TNF-α (GB11188, Servicebio, China), IL-10 (GB11534, Servicebio, China), and VEGF (GB15165, Servicebio, China) to identify differences in local inflammatory and angiogenic profiles.

    Techniques: In Vivo, Modification, Staining, Immunofluorescence, Marker, Fluorescence, Immunohistochemical staining, Expressing, Standard Deviation

    Topical calcitriol application ameliorates IMQ‐induced psoriasis in mice. (A) Schematic illustration of the unilateral ear model experimental design. (B) Serum calcium levels. (C) Body weight changes. (D) Clinical severity scores (erythema, scaling and thickness) of the right ear, assessed on indicated days using a 0–4 scale. Cumulative scores are presented as mean ± SD. (E) Representative photographs of the right ear at endpoint. (F) Haematoxylin and eosin (H&E) staining of right ear sections. Scale bar = 100 μm. (G) Relative mRNA expression levels of IL‐1α, IL‐6, IL‐17A and IL‐23A . Data are presented as mean ± SD. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

    Journal: Journal of Cellular and Molecular Medicine

    Article Title: Downregulating CHI3L2 via the STAT3 Pathway: The Mechanism of Calcitriol in Suppressing Psoriatic Inflammation and Keratinocyte Hyperproliferation

    doi: 10.1111/jcmm.71367

    Figure Lengend Snippet: Topical calcitriol application ameliorates IMQ‐induced psoriasis in mice. (A) Schematic illustration of the unilateral ear model experimental design. (B) Serum calcium levels. (C) Body weight changes. (D) Clinical severity scores (erythema, scaling and thickness) of the right ear, assessed on indicated days using a 0–4 scale. Cumulative scores are presented as mean ± SD. (E) Representative photographs of the right ear at endpoint. (F) Haematoxylin and eosin (H&E) staining of right ear sections. Scale bar = 100 μm. (G) Relative mRNA expression levels of IL‐1α, IL‐6, IL‐17A and IL‐23A . Data are presented as mean ± SD. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

    Article Snippet: To mimic psoriatic keratinocyte dysfunction, HaCaT cells were incubated with 10 ng/mL M5 (IL‐17A, IL‐22, IL‐1α, oncostatin M and TNF‐α) (ABclonal Technology Co. Ltd., Wuhan, China) for 24 h as reported previously [ , , , ].

    Techniques: Staining, Expressing

    Topical calcitriol treatment ameliorates distant psoriatic skin lesions in the bilateral ear model. (A) Schematic illustration of the bilateral ear model experimental design. (B) Serum calcium levels. (C) Body weight changes. (D) Clinical severity scores (erythema, scaling and thickness) of the right ear, assessed on indicated days using a 0–4 scale. Cumulative scores are presented as mean ± SD. (E) Representative photographs of the left ear at endpoint. (F) Haematoxylin and eosin (H&E) staining of left ear sections. Scale bar = 100 μm. (G) Relative mRNA expression levels of IL‐1α, IL‐6, IL‐17A and IL‐23A . Data are presented as mean ± SD. ** p < 0.01, **** p < 0.0001.

    Journal: Journal of Cellular and Molecular Medicine

    Article Title: Downregulating CHI3L2 via the STAT3 Pathway: The Mechanism of Calcitriol in Suppressing Psoriatic Inflammation and Keratinocyte Hyperproliferation

    doi: 10.1111/jcmm.71367

    Figure Lengend Snippet: Topical calcitriol treatment ameliorates distant psoriatic skin lesions in the bilateral ear model. (A) Schematic illustration of the bilateral ear model experimental design. (B) Serum calcium levels. (C) Body weight changes. (D) Clinical severity scores (erythema, scaling and thickness) of the right ear, assessed on indicated days using a 0–4 scale. Cumulative scores are presented as mean ± SD. (E) Representative photographs of the left ear at endpoint. (F) Haematoxylin and eosin (H&E) staining of left ear sections. Scale bar = 100 μm. (G) Relative mRNA expression levels of IL‐1α, IL‐6, IL‐17A and IL‐23A . Data are presented as mean ± SD. ** p < 0.01, **** p < 0.0001.

    Article Snippet: To mimic psoriatic keratinocyte dysfunction, HaCaT cells were incubated with 10 ng/mL M5 (IL‐17A, IL‐22, IL‐1α, oncostatin M and TNF‐α) (ABclonal Technology Co. Ltd., Wuhan, China) for 24 h as reported previously [ , , , ].

    Techniques: Staining, Expressing

    Calcitriol ameliorates M5‐induced abnormal proliferation, migration and inflammatory responses in HaCaT cells. (A) Protein expression levels of KRT1 and KRT6 were determined by Western blot analysis, with β‐Actin serving as the internal loading control. (B) Cell viability was assessed in different treatment groups. (C) Colony formation assay was performed to evaluate the proliferative capacity of cells in each group. (D) Representative images of wound healing assay at 0 and 24 h post‐treatment. Scale bar = 400 μm. (E) Relative mRNA expression levels of IL‐1α, IL‐6, IL‐17A and IL‐23A . Data are presented as mean ± SD. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

    Journal: Journal of Cellular and Molecular Medicine

    Article Title: Downregulating CHI3L2 via the STAT3 Pathway: The Mechanism of Calcitriol in Suppressing Psoriatic Inflammation and Keratinocyte Hyperproliferation

    doi: 10.1111/jcmm.71367

    Figure Lengend Snippet: Calcitriol ameliorates M5‐induced abnormal proliferation, migration and inflammatory responses in HaCaT cells. (A) Protein expression levels of KRT1 and KRT6 were determined by Western blot analysis, with β‐Actin serving as the internal loading control. (B) Cell viability was assessed in different treatment groups. (C) Colony formation assay was performed to evaluate the proliferative capacity of cells in each group. (D) Representative images of wound healing assay at 0 and 24 h post‐treatment. Scale bar = 400 μm. (E) Relative mRNA expression levels of IL‐1α, IL‐6, IL‐17A and IL‐23A . Data are presented as mean ± SD. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

    Article Snippet: To mimic psoriatic keratinocyte dysfunction, HaCaT cells were incubated with 10 ng/mL M5 (IL‐17A, IL‐22, IL‐1α, oncostatin M and TNF‐α) (ABclonal Technology Co. Ltd., Wuhan, China) for 24 h as reported previously [ , , , ].

    Techniques: Migration, Expressing, Western Blot, Control, Colony Assay, Wound Healing Assay

    Calcitriol ameliorates M5‐induced psoriasis‐like phenotypes through CHI3L2 downregulation. (A) The mRNA expression of RPL36A, PPBP, UBE2F, MGC32805, IL4I1, LINC00519, CHI3L2, ABHD14A and PCDHGB7 , validated by RT‐qPCR assay. (B) Efficacy of shRNA‐mediated CHI3L2 knockdown confirmed by RT‐qPCR. (C) Protein expression levels of KRT1 and KRT6 were determined by Western blot analysis, with β‐Actin serving as the internal loading control. (D) Cell viability was assessed in different treatment groups. (E) Representative images of wound healing assay at 0 and 24 h post‐treatment. Scale bar = 400 μm. (F) Relative mRNA expression levels of IL‐1α, IL‐6, IL‐17A and IL‐23A . Data are presented as mean ± SD. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

    Journal: Journal of Cellular and Molecular Medicine

    Article Title: Downregulating CHI3L2 via the STAT3 Pathway: The Mechanism of Calcitriol in Suppressing Psoriatic Inflammation and Keratinocyte Hyperproliferation

    doi: 10.1111/jcmm.71367

    Figure Lengend Snippet: Calcitriol ameliorates M5‐induced psoriasis‐like phenotypes through CHI3L2 downregulation. (A) The mRNA expression of RPL36A, PPBP, UBE2F, MGC32805, IL4I1, LINC00519, CHI3L2, ABHD14A and PCDHGB7 , validated by RT‐qPCR assay. (B) Efficacy of shRNA‐mediated CHI3L2 knockdown confirmed by RT‐qPCR. (C) Protein expression levels of KRT1 and KRT6 were determined by Western blot analysis, with β‐Actin serving as the internal loading control. (D) Cell viability was assessed in different treatment groups. (E) Representative images of wound healing assay at 0 and 24 h post‐treatment. Scale bar = 400 μm. (F) Relative mRNA expression levels of IL‐1α, IL‐6, IL‐17A and IL‐23A . Data are presented as mean ± SD. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

    Article Snippet: To mimic psoriatic keratinocyte dysfunction, HaCaT cells were incubated with 10 ng/mL M5 (IL‐17A, IL‐22, IL‐1α, oncostatin M and TNF‐α) (ABclonal Technology Co. Ltd., Wuhan, China) for 24 h as reported previously [ , , , ].

    Techniques: Expressing, Quantitative RT-PCR, shRNA, Knockdown, Western Blot, Control, Wound Healing Assay

    Quantitative detection of LPS-induced inflammatory mediators after treatment with CGAA, CGA, CGL and positive control epalrestat in RAW264.7 macrophages. ( a , b ) Determination of NO production: ( a ) Full concentration–response profiles at 10–100 μM. ( b ) Single-dose comparison at 100 μM. ( c , d ) Quantification of IL-6 secretion: ( c ) Full concentration–response profiles at 10–100 μM. ( d ) Single-dose comparison at 100 μM. ( e , f ) Quantification of TNF-α secretion: ( e ) Full concentration–response profiles at 10–100 μM. ( f ) Single-dose comparison at 100 μM. Cells were pretreated with the indicated compounds (10–100 μM) for 2 h, followed by LPS (1 μg/mL) stimulation for 24 h. NO levels were determined via the Griess assay, while IL-6 and TNF-α concentrations were quantified by ELISA. All data are expressed as mean ± SD ( n = 3). #### p < 0.0001 vs. the control group; **** p < 0.0001, *** p < 0.001, ** p < 0.01, * p < 0.05 vs. the LPS group.

    Journal: Molecules

    Article Title: Carboxyl Amidation of Chlorogenic Acid Improves Anti-Inflammatory Activity and Biosafety via Potent AKR1B1 Inhibition in LPS-Induced Macrophages

    doi: 10.3390/molecules31183247

    Figure Lengend Snippet: Quantitative detection of LPS-induced inflammatory mediators after treatment with CGAA, CGA, CGL and positive control epalrestat in RAW264.7 macrophages. ( a , b ) Determination of NO production: ( a ) Full concentration–response profiles at 10–100 μM. ( b ) Single-dose comparison at 100 μM. ( c , d ) Quantification of IL-6 secretion: ( c ) Full concentration–response profiles at 10–100 μM. ( d ) Single-dose comparison at 100 μM. ( e , f ) Quantification of TNF-α secretion: ( e ) Full concentration–response profiles at 10–100 μM. ( f ) Single-dose comparison at 100 μM. Cells were pretreated with the indicated compounds (10–100 μM) for 2 h, followed by LPS (1 μg/mL) stimulation for 24 h. NO levels were determined via the Griess assay, while IL-6 and TNF-α concentrations were quantified by ELISA. All data are expressed as mean ± SD ( n = 3). #### p < 0.0001 vs. the control group; **** p < 0.0001, *** p < 0.001, ** p < 0.01, * p < 0.05 vs. the LPS group.

    Article Snippet: The levels of TNF-α and IL-6 in culture supernatants were quantified using commercial ELISA kits (Mouse TNF-alpha Fast Pro ELISA Kit, Cat. No. RK05228; Mouse IL-6 Fast Pro ELISA Kit, Cat. No. RK05213; ABclonal, Wuhan, China).

    Techniques: Positive Control, Concentration Assay, Comparison, Griess Assay, Enzyme-linked Immunosorbent Assay, Control

    Temperature-gradient CETSA analysis of AKR1B1. Cell lysates pretreated with CGA, CGL, or CGAA were heated at 4, 45, 60, 75, or 90 °C. Residual soluble AKR1B1 protein was quantified by ELISA and normalized to the corresponding 4 °C sample. Data are presented as mean ± SD ( n = 3). **** p < 0.0001 vs. the CGA group.

    Journal: Molecules

    Article Title: Carboxyl Amidation of Chlorogenic Acid Improves Anti-Inflammatory Activity and Biosafety via Potent AKR1B1 Inhibition in LPS-Induced Macrophages

    doi: 10.3390/molecules31183247

    Figure Lengend Snippet: Temperature-gradient CETSA analysis of AKR1B1. Cell lysates pretreated with CGA, CGL, or CGAA were heated at 4, 45, 60, 75, or 90 °C. Residual soluble AKR1B1 protein was quantified by ELISA and normalized to the corresponding 4 °C sample. Data are presented as mean ± SD ( n = 3). **** p < 0.0001 vs. the CGA group.

    Article Snippet: The levels of TNF-α and IL-6 in culture supernatants were quantified using commercial ELISA kits (Mouse TNF-alpha Fast Pro ELISA Kit, Cat. No. RK05228; Mouse IL-6 Fast Pro ELISA Kit, Cat. No. RK05213; ABclonal, Wuhan, China).

    Techniques: Analysis, Enzyme-linked Immunosorbent Assay

    SGF inhibits hepatic glycolysis and AIM2 inflammasome activation in HFD-fed mice. (A, B) Protein expression of HK2, PKM2 and LDHA in the liver. (C, D) Lactate and pyruvate expression in the liver. (E, F) Protein expression of AIM2, ASC, Caspase-1 and IL-1β in the liver. (G, H) ELISA measurement of serum IL-1β and TNF-α levels. (I) mRNA expression levels of IL-1β, IL-18, IL-6, and TNF-α. (J) AIM2 inflammasome fluorescence colocalization images. Data are presented as the mean ± SD (n = 3-6). * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 vs. control; # p < 0.05, ## p < 0.01, ### p < 0.001, #### p < 0.0001 vs. model.

    Journal: Frontiers in Immunology

    Article Title: Smilax glabra flavonoids ameliorate non-alcoholic steatohepatitis by regulating PKM2-dependent glycolysis and suppressing AIM2 inflammasome activation

    doi: 10.3389/fimmu.2026.1906439

    Figure Lengend Snippet: SGF inhibits hepatic glycolysis and AIM2 inflammasome activation in HFD-fed mice. (A, B) Protein expression of HK2, PKM2 and LDHA in the liver. (C, D) Lactate and pyruvate expression in the liver. (E, F) Protein expression of AIM2, ASC, Caspase-1 and IL-1β in the liver. (G, H) ELISA measurement of serum IL-1β and TNF-α levels. (I) mRNA expression levels of IL-1β, IL-18, IL-6, and TNF-α. (J) AIM2 inflammasome fluorescence colocalization images. Data are presented as the mean ± SD (n = 3-6). * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 vs. control; # p < 0.05, ## p < 0.01, ### p < 0.001, #### p < 0.0001 vs. model.

    Article Snippet: Serum levels of tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) were determined using ELISA kits (ABclonal Biotech Co., Ltd, China).

    Techniques: Activation Assay, Expressing, Enzyme-linked Immunosorbent Assay, Fluorescence, Control