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rabbit tnf α polyclonal antibody bioss antibodies  (Bioss)


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    Bioss rabbit tnf α polyclonal antibody bioss antibodies
    Rabbit Tnf α Polyclonal Antibody Bioss Antibodies, supplied by Bioss, used in various techniques. Bioz Stars score: 95/100, based on 114 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 95 stars, based on 114 article reviews
    rabbit tnf α polyclonal antibody bioss antibodies - by Bioz Stars, 2026-03
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    Multi Sciences (Lianke) Biotech Co Ltd mouse tnf α
    | In vivo anti-oxidant and anti-inflammatory effects of NTAl NPs against UC. A) H&E-stained sections of mouse colon following treatment with indicated materials. B) H&E staining histological scores. C) Typical TEM images showing the microstructures of colonic epitheliums. D-F) the expression of oxidative stress markers including MDA(D), SOD (E), and GSH-Px (F). G-J) the expression of colonic inflammatory cytokines including pro-inflammatory <t>cytokines</t> <t>TNF-α</t> (G), IL-1β (H), IL-6 (I) and anti-inflammatory cytokines IL-10 (J). All data are shown as mean ± s.d; n = 6. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001.
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    Proteintech tnf α recombinant antibody
    The regulatory effects of CaHA/PLGA microspheres on macrophages and ADSCs in vitro. (A, B) CLSM images and RFI of CD86 and CD206 expression in RAW264.7 cells co-cultured with microspheres for 2 days (n = 3). (C–F) Relative mRNA expression levels of inflammation-related genes <t>TNF-α,</t> IL-6, TGF-β1, and FGF-2 in RAW264.7 cells (n = 3). (G, H) Sirius red staining images and quantitative analysis (n = 3) of collagen deposition of ADSCs co-cultured with CaHA/PLGA microspheres for 3 and 7 days. (I–K) Relative mRNA expression levels of TGF-β1, FGF-2, and PDGF-A in ADSCs after 3 and 7 days of co-culture with CaHA/PLGA microspheres (n = 3). ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001; ∗∗∗∗ p < 0.0001; ns , not significant.
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    Significant Ups genes in the acetabular cartilage of the rats with DDH, as determined by mRNA-seq analysis. (A) Neonatal rats were subjected to straight-leg swaddling for 10 days. A total of 4 weeks later, (a) morphology, (b) H&E staining and (c) SO/FG staining were assessed in the hip joints of the rats. (B) Immunohistochemical staining and (E) semi-quantitative analysis of COL2A1 in the acetabular cartilage of the 4-week-old control rats and rats with DDH. (C) Relative gene expression levels of COL2A1, IL-1β and IL-6 in the acetabular cartilage of the 4-week-old control rats and rats with DDH, as determined by reverse transcription-quantitative PCR. (D) Levels of IL-6 in the supernatants of acetabular cartilage from the 4-week-old rats with DDH, as determined by <t>ELISA.</t> (F) Significant Ups in the acetabular cartilage of rats with DDH were identified by mRNA-seq analysis with the screening criteria of log 2 FC >4 and P.adj<0.01. Principal component analysis results and a heatmap of these significant Ups are shown. (G) GO enrichment analysis of significant Ups in the acetabular cartilage of the rats with DDH. Data are presented as the mean ± SD. *** P<0.001. (C-E) Representative results of four independent experiments are shown. Ups, upregulated genes; BP, biological process; CC, cellular component; COL2A1, type II collagen; DDH, developmental dysplasia of the hip; FC, fold change; GO, Gene Ontology; H&E, hematoxylin and eosin; IHC, immunohistochemistry; IL, interleukin; IOD, integrated optical density; MF, molecular function; mRNA-seq, mRNA sequencing; SO/FG, Safranin O/Fast Green.
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    MedChemExpress hy p1860
    Significant Ups genes in the acetabular cartilage of the rats with DDH, as determined by mRNA-seq analysis. (A) Neonatal rats were subjected to straight-leg swaddling for 10 days. A total of 4 weeks later, (a) morphology, (b) H&E staining and (c) SO/FG staining were assessed in the hip joints of the rats. (B) Immunohistochemical staining and (E) semi-quantitative analysis of COL2A1 in the acetabular cartilage of the 4-week-old control rats and rats with DDH. (C) Relative gene expression levels of COL2A1, IL-1β and IL-6 in the acetabular cartilage of the 4-week-old control rats and rats with DDH, as determined by reverse transcription-quantitative PCR. (D) Levels of IL-6 in the supernatants of acetabular cartilage from the 4-week-old rats with DDH, as determined by <t>ELISA.</t> (F) Significant Ups in the acetabular cartilage of rats with DDH were identified by mRNA-seq analysis with the screening criteria of log 2 FC >4 and P.adj<0.01. Principal component analysis results and a heatmap of these significant Ups are shown. (G) GO enrichment analysis of significant Ups in the acetabular cartilage of the rats with DDH. Data are presented as the mean ± SD. *** P<0.001. (C-E) Representative results of four independent experiments are shown. Ups, upregulated genes; BP, biological process; CC, cellular component; COL2A1, type II collagen; DDH, developmental dysplasia of the hip; FC, fold change; GO, Gene Ontology; H&E, hematoxylin and eosin; IHC, immunohistochemistry; IL, interleukin; IOD, integrated optical density; MF, molecular function; mRNA-seq, mRNA sequencing; SO/FG, Safranin O/Fast Green.
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    Treprostinil promotes endothelial cell survival and viability (A) TUNEL staining showed that treprostinil significantly inhibited the apoptosis of human umbilical vein endothelial cells (HUVECs) induced by tumor <t>necrosis</t> <t>factor-α</t> ( n = 3 biological samples per group). Scale bars, 50 μm (B–D) CCK8 and qPCR analyses suggested that treprostinil promoted cell viability and reduced inflammation in HUVECs ( n = 6 biological samples per group). Two-tailed unpaired Student’s t test was used to calculate statistical significance. Data are represented as mean ± SEM. ∗ represents p < 0.05, ∗∗ represents p < 0.01, and ∗∗∗ represents p < 0.001.
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    Effects of WYTLG on inflammatory factors and apoptosis in GIM rats. A Relative mRNA expression levels of pro-inflammatory cytokines ( Il1b , Il6 , Tnfα , Ptgs2 ) and anti-inflammatory cytokines ( Il10 , Tgfb ) in gastric tissues. B-E Serum levels of pro-inflammatory (IL-1β, <t>IL-6,</t> <t>TNF-α)</t> and anti-inflammatory (IL-10) cytokines. F, G TUNEL staining and semi-quantitative analysis of apoptotic cells (scale bar = 50 μm). H, I Western blot analysis of cytochrome c, Bax/Bcl-2, and cleaved caspase-3 protein expression. ( n = 3–8). # p < 0.05, ## p < 0.01, ### p < 0.001 vs. control group; * p < 0.05, ** p < 0.01, *** p < 0.001 vs. model group
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    Thermo Fisher gene exp tnf hs00174128 m1
    Hyperinflammatory cytokine and IFN responses in patient PBMCs. (A–H) PBMCs from the patient (red) and three controls (grey) were left untreated (UT), stimulated with TLR4 agonist LPS, TLR7/8 agonist R848, transfected with PolyIC for TLR3/MDA5/RIG-I stimulation, or mock transfected (transf ctrl). Cells were harvested 24 h after treatment, and RNA was isolated and analyzed for IFNB1 (B), CXCL10 (C), IL6 (D), and <t>TNF</t> (E) gene transcription by RT-PCR, and cell culture supernatants were collected and analyzed for CXCL10 (F), IL6 (G), and TNF (H) protein by ELISA. Bars indicate mean values ± standard deviation (SD) of a single experiment performed in triplicates. Statistics were calculated using the ordinary One-way ANOVA with Šídák’s multiple comparisons test. * = P < 0.05, ** = P < 0.01, *** = P < 0.001, **** = P < 0.0001, and ns = not significant.
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    Bioss rabbit tnf α polyclonal antibody bioss antibodies
    Hyperinflammatory cytokine and IFN responses in patient PBMCs. (A–H) PBMCs from the patient (red) and three controls (grey) were left untreated (UT), stimulated with TLR4 agonist LPS, TLR7/8 agonist R848, transfected with PolyIC for TLR3/MDA5/RIG-I stimulation, or mock transfected (transf ctrl). Cells were harvested 24 h after treatment, and RNA was isolated and analyzed for IFNB1 (B), CXCL10 (C), IL6 (D), and <t>TNF</t> (E) gene transcription by RT-PCR, and cell culture supernatants were collected and analyzed for CXCL10 (F), IL6 (G), and TNF (H) protein by ELISA. Bars indicate mean values ± standard deviation (SD) of a single experiment performed in triplicates. Statistics were calculated using the ordinary One-way ANOVA with Šídák’s multiple comparisons test. * = P < 0.05, ** = P < 0.01, *** = P < 0.001, **** = P < 0.0001, and ns = not significant.
    Rabbit Tnf α Polyclonal Antibody Bioss Antibodies, supplied by Bioss, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    MedChemExpress tnf α inhibitor etanercept
    Single-cell transcriptome analysis highlight predominant role of neutrophil-derived TNF signaling in mediating immune-chondrocyte interaction in the APC-exposed condyles. a Circle plot of TNF signaling network. b Bubble plot of the communication probability of all the significant ligand-receptor pairs that contributed to increasing signaling sent from Stage II neutrophils to each cell population in chondrocytes. c Co-immunofluorescence staining of the condyle for Myeloperoxidase (MPO, green) <t>and</t> <t>TNF-α</t> (red), or for CD68 (green) and TNF-α (red). Co-localization of MPO and TNF-α indicates production of TNF-α from neutrophils. Scale bar: 50 μm for the low-power field, 10 μm for the high-power field. d Semi-quantitation of the expression levels of MPO, CD68 and TNF-α. * P < 0.05. ** P < 0.01. *** P < 0.001. **** P < 0.000 1
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    Image Search Results


    | In vivo anti-oxidant and anti-inflammatory effects of NTAl NPs against UC. A) H&E-stained sections of mouse colon following treatment with indicated materials. B) H&E staining histological scores. C) Typical TEM images showing the microstructures of colonic epitheliums. D-F) the expression of oxidative stress markers including MDA(D), SOD (E), and GSH-Px (F). G-J) the expression of colonic inflammatory cytokines including pro-inflammatory cytokines TNF-α (G), IL-1β (H), IL-6 (I) and anti-inflammatory cytokines IL-10 (J). All data are shown as mean ± s.d; n = 6. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001.

    Journal: Materials Today Bio

    Article Title: One-step green assembly of natural polyphenol-based nobiletin nanoparticles for ulcerative colitis therapy

    doi: 10.1016/j.mtbio.2026.102887

    Figure Lengend Snippet: | In vivo anti-oxidant and anti-inflammatory effects of NTAl NPs against UC. A) H&E-stained sections of mouse colon following treatment with indicated materials. B) H&E staining histological scores. C) Typical TEM images showing the microstructures of colonic epitheliums. D-F) the expression of oxidative stress markers including MDA(D), SOD (E), and GSH-Px (F). G-J) the expression of colonic inflammatory cytokines including pro-inflammatory cytokines TNF-α (G), IL-1β (H), IL-6 (I) and anti-inflammatory cytokines IL-10 (J). All data are shown as mean ± s.d; n = 6. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001.

    Article Snippet: Commercial ELISA kits including Mouse TNF-α (EK282, Multi Sciences), Mouse IL-1β (EK201B, Multi Sciences), Mouse IL-6 (EK206, Multi Sciences), and Mouse IL-10 (EK210, Multi Sciences) were used to quantify pro-inflammatory cytokines and the anti-inflammatory cytokine according to the manufacturer's instructions.

    Techniques: In Vivo, Staining, Expressing

    The regulatory effects of CaHA/PLGA microspheres on macrophages and ADSCs in vitro. (A, B) CLSM images and RFI of CD86 and CD206 expression in RAW264.7 cells co-cultured with microspheres for 2 days (n = 3). (C–F) Relative mRNA expression levels of inflammation-related genes TNF-α, IL-6, TGF-β1, and FGF-2 in RAW264.7 cells (n = 3). (G, H) Sirius red staining images and quantitative analysis (n = 3) of collagen deposition of ADSCs co-cultured with CaHA/PLGA microspheres for 3 and 7 days. (I–K) Relative mRNA expression levels of TGF-β1, FGF-2, and PDGF-A in ADSCs after 3 and 7 days of co-culture with CaHA/PLGA microspheres (n = 3). ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001; ∗∗∗∗ p < 0.0001; ns , not significant.

    Journal: Bioactive Materials

    Article Title: Mossy-textured hydroxyapatite-modified poly (lactic-co-glycolic acid) microspheres promote collagen regeneration via calcium/TGF-β and chemokine signaling pathways in soft tissue augmentation

    doi: 10.1016/j.bioactmat.2025.12.028

    Figure Lengend Snippet: The regulatory effects of CaHA/PLGA microspheres on macrophages and ADSCs in vitro. (A, B) CLSM images and RFI of CD86 and CD206 expression in RAW264.7 cells co-cultured with microspheres for 2 days (n = 3). (C–F) Relative mRNA expression levels of inflammation-related genes TNF-α, IL-6, TGF-β1, and FGF-2 in RAW264.7 cells (n = 3). (G, H) Sirius red staining images and quantitative analysis (n = 3) of collagen deposition of ADSCs co-cultured with CaHA/PLGA microspheres for 3 and 7 days. (I–K) Relative mRNA expression levels of TGF-β1, FGF-2, and PDGF-A in ADSCs after 3 and 7 days of co-culture with CaHA/PLGA microspheres (n = 3). ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001; ∗∗∗∗ p < 0.0001; ns , not significant.

    Article Snippet: CD86 polyclonal antibody (1:200, 13395-1-AP, Proteintech), CD206 (1:200, 18704-1-AP, Proteintech), and TNF-α recombinant antibody (1:200, 80258-6-RR, Proteintech) were used as primary antibodies, incubated overnight at 4 °C.

    Techniques: In Vitro, Expressing, Cell Culture, Staining, Co-Culture Assay

    Evaluation of soft tissue filling and inflammatory response in rats. (A, B) Schematic diagram of the soft tissue filling experiment and injection sites, with at least 2 cm spacing between sites. (C) Photographs of subcutaneous soft tissue filling at 2, 4, 8, and 12 weeks. The white circles indicate the soft tissue filling areas. (D) H&E staining of the filled sites. (E, F) Immunofluorescence images and RFI of TNF-α and TGF-β expression at 2 weeks post-filling (n = 6). (G, H) Immunofluorescence images and RFI of CD86 and CD206 expression at 2 weeks post-filling (n = 6). ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001; ∗∗∗∗ p < 0.0001; ns , not significant.

    Journal: Bioactive Materials

    Article Title: Mossy-textured hydroxyapatite-modified poly (lactic-co-glycolic acid) microspheres promote collagen regeneration via calcium/TGF-β and chemokine signaling pathways in soft tissue augmentation

    doi: 10.1016/j.bioactmat.2025.12.028

    Figure Lengend Snippet: Evaluation of soft tissue filling and inflammatory response in rats. (A, B) Schematic diagram of the soft tissue filling experiment and injection sites, with at least 2 cm spacing between sites. (C) Photographs of subcutaneous soft tissue filling at 2, 4, 8, and 12 weeks. The white circles indicate the soft tissue filling areas. (D) H&E staining of the filled sites. (E, F) Immunofluorescence images and RFI of TNF-α and TGF-β expression at 2 weeks post-filling (n = 6). (G, H) Immunofluorescence images and RFI of CD86 and CD206 expression at 2 weeks post-filling (n = 6). ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001; ∗∗∗∗ p < 0.0001; ns , not significant.

    Article Snippet: CD86 polyclonal antibody (1:200, 13395-1-AP, Proteintech), CD206 (1:200, 18704-1-AP, Proteintech), and TNF-α recombinant antibody (1:200, 80258-6-RR, Proteintech) were used as primary antibodies, incubated overnight at 4 °C.

    Techniques: Injection, Staining, Immunofluorescence, Expressing

    Significant Ups genes in the acetabular cartilage of the rats with DDH, as determined by mRNA-seq analysis. (A) Neonatal rats were subjected to straight-leg swaddling for 10 days. A total of 4 weeks later, (a) morphology, (b) H&E staining and (c) SO/FG staining were assessed in the hip joints of the rats. (B) Immunohistochemical staining and (E) semi-quantitative analysis of COL2A1 in the acetabular cartilage of the 4-week-old control rats and rats with DDH. (C) Relative gene expression levels of COL2A1, IL-1β and IL-6 in the acetabular cartilage of the 4-week-old control rats and rats with DDH, as determined by reverse transcription-quantitative PCR. (D) Levels of IL-6 in the supernatants of acetabular cartilage from the 4-week-old rats with DDH, as determined by ELISA. (F) Significant Ups in the acetabular cartilage of rats with DDH were identified by mRNA-seq analysis with the screening criteria of log 2 FC >4 and P.adj<0.01. Principal component analysis results and a heatmap of these significant Ups are shown. (G) GO enrichment analysis of significant Ups in the acetabular cartilage of the rats with DDH. Data are presented as the mean ± SD. *** P<0.001. (C-E) Representative results of four independent experiments are shown. Ups, upregulated genes; BP, biological process; CC, cellular component; COL2A1, type II collagen; DDH, developmental dysplasia of the hip; FC, fold change; GO, Gene Ontology; H&E, hematoxylin and eosin; IHC, immunohistochemistry; IL, interleukin; IOD, integrated optical density; MF, molecular function; mRNA-seq, mRNA sequencing; SO/FG, Safranin O/Fast Green.

    Journal: International Journal of Molecular Medicine

    Article Title: DUSP26: Unveiling a critical molecular mediator and therapeutic target in developmental dysplasia of the hip-associated secondary osteoarthritis

    doi: 10.3892/ijmm.2026.5776

    Figure Lengend Snippet: Significant Ups genes in the acetabular cartilage of the rats with DDH, as determined by mRNA-seq analysis. (A) Neonatal rats were subjected to straight-leg swaddling for 10 days. A total of 4 weeks later, (a) morphology, (b) H&E staining and (c) SO/FG staining were assessed in the hip joints of the rats. (B) Immunohistochemical staining and (E) semi-quantitative analysis of COL2A1 in the acetabular cartilage of the 4-week-old control rats and rats with DDH. (C) Relative gene expression levels of COL2A1, IL-1β and IL-6 in the acetabular cartilage of the 4-week-old control rats and rats with DDH, as determined by reverse transcription-quantitative PCR. (D) Levels of IL-6 in the supernatants of acetabular cartilage from the 4-week-old rats with DDH, as determined by ELISA. (F) Significant Ups in the acetabular cartilage of rats with DDH were identified by mRNA-seq analysis with the screening criteria of log 2 FC >4 and P.adj<0.01. Principal component analysis results and a heatmap of these significant Ups are shown. (G) GO enrichment analysis of significant Ups in the acetabular cartilage of the rats with DDH. Data are presented as the mean ± SD. *** P<0.001. (C-E) Representative results of four independent experiments are shown. Ups, upregulated genes; BP, biological process; CC, cellular component; COL2A1, type II collagen; DDH, developmental dysplasia of the hip; FC, fold change; GO, Gene Ontology; H&E, hematoxylin and eosin; IHC, immunohistochemistry; IL, interleukin; IOD, integrated optical density; MF, molecular function; mRNA-seq, mRNA sequencing; SO/FG, Safranin O/Fast Green.

    Article Snippet: Protein concentrations were measured using a BCA assay kit (cat. no. PK10026; Wuhan Sanying Biotechnology), and the levels of TNF-α and IL-6 in the tissue homogenates and cell supernatants were measured using the Rat TNF-α ELISA Kit (cat. no. EK382; Multi Sciences Biotech) and Rat IL-6 ELISA Kit (cat. no. EK306; Multi Sciences Biotech), according to the manufacturers' instructions.

    Techniques: Staining, Immunohistochemical staining, Control, Gene Expression, Reverse Transcription, Real-time Polymerase Chain Reaction, Enzyme-linked Immunosorbent Assay, Immunohistochemistry, Sequencing

    DUSP26 overexpression alleviates IL-1β-induced chondrocyte injury. Rat DUSP26 overexpression adenovirus was constructed and used to infect chondrocytes. After 24 h, the chondrocytes were subjected to 10 ng/ml IL-1β. (A) Expression levels of COL2A1 and COL1A1 in the chondrocytes were detected by RT-qPCR and western blotting. (B) Relative mRNA expression levels of TNF-α and IL-6 in the chondrocytes were determined by RT-qPCR. (C) Levels of TNF-α and IL-6 in the supernatants of the chondrocytes were determined by ELISA. Two adenovirus-mediated shRNAs against rat DUSP26 were constructed and used to infect chondrocytes. After 24 h, the chondrocytes were subjected to 10 ng/ml IL-1β. (D) Expression levels of COL2A1 and COL1A1 in the chondrocytes were evaluated by RT-qPCR and western blotting. (E) Relative mRNA expression levels of TNF-α and IL-6 in the chondrocytes were determined by RT-qPCR. (F) Levels of TNF-α and IL-6 in the supernatants of the chondrocytes were detected by ELISA. Data are presented as the mean ± SD. * P<0.05, ** P<0.01 and *** P<0.001. Representative results of three independent experiments are shown. COL1A1, type I collagen; COL2A1, type II collagen; EP, empty adenoviral vector; DUSP26, dual-specificity phosphatase 26; IL, interleukin; NC, negative control; RT-qPCR, reverse transcription-quantitative PCR; sh, short hairpin.

    Journal: International Journal of Molecular Medicine

    Article Title: DUSP26: Unveiling a critical molecular mediator and therapeutic target in developmental dysplasia of the hip-associated secondary osteoarthritis

    doi: 10.3892/ijmm.2026.5776

    Figure Lengend Snippet: DUSP26 overexpression alleviates IL-1β-induced chondrocyte injury. Rat DUSP26 overexpression adenovirus was constructed and used to infect chondrocytes. After 24 h, the chondrocytes were subjected to 10 ng/ml IL-1β. (A) Expression levels of COL2A1 and COL1A1 in the chondrocytes were detected by RT-qPCR and western blotting. (B) Relative mRNA expression levels of TNF-α and IL-6 in the chondrocytes were determined by RT-qPCR. (C) Levels of TNF-α and IL-6 in the supernatants of the chondrocytes were determined by ELISA. Two adenovirus-mediated shRNAs against rat DUSP26 were constructed and used to infect chondrocytes. After 24 h, the chondrocytes were subjected to 10 ng/ml IL-1β. (D) Expression levels of COL2A1 and COL1A1 in the chondrocytes were evaluated by RT-qPCR and western blotting. (E) Relative mRNA expression levels of TNF-α and IL-6 in the chondrocytes were determined by RT-qPCR. (F) Levels of TNF-α and IL-6 in the supernatants of the chondrocytes were detected by ELISA. Data are presented as the mean ± SD. * P<0.05, ** P<0.01 and *** P<0.001. Representative results of three independent experiments are shown. COL1A1, type I collagen; COL2A1, type II collagen; EP, empty adenoviral vector; DUSP26, dual-specificity phosphatase 26; IL, interleukin; NC, negative control; RT-qPCR, reverse transcription-quantitative PCR; sh, short hairpin.

    Article Snippet: Protein concentrations were measured using a BCA assay kit (cat. no. PK10026; Wuhan Sanying Biotechnology), and the levels of TNF-α and IL-6 in the tissue homogenates and cell supernatants were measured using the Rat TNF-α ELISA Kit (cat. no. EK382; Multi Sciences Biotech) and Rat IL-6 ELISA Kit (cat. no. EK306; Multi Sciences Biotech), according to the manufacturers' instructions.

    Techniques: Over Expression, Construct, Expressing, Quantitative RT-PCR, Western Blot, Enzyme-linked Immunosorbent Assay, Plasmid Preparation, Negative Control, Reverse Transcription, Real-time Polymerase Chain Reaction

    Inactivation of HDAC1/2/8 inhibits DUSP26 silencing-triggered cartilage degeneration. (A) Total protein and phosphorylation levels of HDAC1, HDAC2 and HDAC8 in IL-1β-treated chondrocytes determined by western blotting. (B) Relative mRNA expression levels of HDAC1, HDAC2 and HDAC8 in chondrocytes, as determined by reverse transcription-quantitative PCR. (C) Relative mRNA expression levels of COL1A1 and TNF-α in IL-1β-treated chondrocytes after knocking down HDAC1/2/8. (D) Relative mRNA expression levels of COL1A1 and TNF-α in IL-1β-treated chondrocytes after intervention with the HDAC inhibitor TSA. (E) Protein levels of COL1A1 and TNF-α in IL-1β-treated chondrocytes after knocking down HDAC1/2/8. (F) Protein levels of COL1A1 and TNF-α in IL-1β-treated chondrocytes after intervention with the HDAC inhibitor TSA. Data are presented as the mean ± SD. * P<0.05, ** P<0.01 and *** P<0.001. (B-D) Representative results of three independent experiments are shown. COL1A1, type I collagen; DUSP26, dual-specificity phosphatase 26; HDAC, histone deacetylase; IL, interleukin; NC, negative control; ns, no significance; sh, short hairpin; TSA, trichostatin A.

    Journal: International Journal of Molecular Medicine

    Article Title: DUSP26: Unveiling a critical molecular mediator and therapeutic target in developmental dysplasia of the hip-associated secondary osteoarthritis

    doi: 10.3892/ijmm.2026.5776

    Figure Lengend Snippet: Inactivation of HDAC1/2/8 inhibits DUSP26 silencing-triggered cartilage degeneration. (A) Total protein and phosphorylation levels of HDAC1, HDAC2 and HDAC8 in IL-1β-treated chondrocytes determined by western blotting. (B) Relative mRNA expression levels of HDAC1, HDAC2 and HDAC8 in chondrocytes, as determined by reverse transcription-quantitative PCR. (C) Relative mRNA expression levels of COL1A1 and TNF-α in IL-1β-treated chondrocytes after knocking down HDAC1/2/8. (D) Relative mRNA expression levels of COL1A1 and TNF-α in IL-1β-treated chondrocytes after intervention with the HDAC inhibitor TSA. (E) Protein levels of COL1A1 and TNF-α in IL-1β-treated chondrocytes after knocking down HDAC1/2/8. (F) Protein levels of COL1A1 and TNF-α in IL-1β-treated chondrocytes after intervention with the HDAC inhibitor TSA. Data are presented as the mean ± SD. * P<0.05, ** P<0.01 and *** P<0.001. (B-D) Representative results of three independent experiments are shown. COL1A1, type I collagen; DUSP26, dual-specificity phosphatase 26; HDAC, histone deacetylase; IL, interleukin; NC, negative control; ns, no significance; sh, short hairpin; TSA, trichostatin A.

    Article Snippet: Protein concentrations were measured using a BCA assay kit (cat. no. PK10026; Wuhan Sanying Biotechnology), and the levels of TNF-α and IL-6 in the tissue homogenates and cell supernatants were measured using the Rat TNF-α ELISA Kit (cat. no. EK382; Multi Sciences Biotech) and Rat IL-6 ELISA Kit (cat. no. EK306; Multi Sciences Biotech), according to the manufacturers' instructions.

    Techniques: Phospho-proteomics, Western Blot, Expressing, Reverse Transcription, Real-time Polymerase Chain Reaction, Histone Deacetylase Assay, Negative Control

    Treprostinil promotes endothelial cell survival and viability (A) TUNEL staining showed that treprostinil significantly inhibited the apoptosis of human umbilical vein endothelial cells (HUVECs) induced by tumor necrosis factor-α ( n = 3 biological samples per group). Scale bars, 50 μm (B–D) CCK8 and qPCR analyses suggested that treprostinil promoted cell viability and reduced inflammation in HUVECs ( n = 6 biological samples per group). Two-tailed unpaired Student’s t test was used to calculate statistical significance. Data are represented as mean ± SEM. ∗ represents p < 0.05, ∗∗ represents p < 0.01, and ∗∗∗ represents p < 0.001.

    Journal: iScience

    Article Title: Development of immune-derived molecular markers for coronary heart disease via multimachine learning

    doi: 10.1016/j.isci.2026.114853

    Figure Lengend Snippet: Treprostinil promotes endothelial cell survival and viability (A) TUNEL staining showed that treprostinil significantly inhibited the apoptosis of human umbilical vein endothelial cells (HUVECs) induced by tumor necrosis factor-α ( n = 3 biological samples per group). Scale bars, 50 μm (B–D) CCK8 and qPCR analyses suggested that treprostinil promoted cell viability and reduced inflammation in HUVECs ( n = 6 biological samples per group). Two-tailed unpaired Student’s t test was used to calculate statistical significance. Data are represented as mean ± SEM. ∗ represents p < 0.05, ∗∗ represents p < 0.01, and ∗∗∗ represents p < 0.001.

    Article Snippet: Tumor necrosis factor-α , MedChemExpress , HY-P1860.

    Techniques: TUNEL Assay, Staining, Two Tailed Test

    Effects of WYTLG on inflammatory factors and apoptosis in GIM rats. A Relative mRNA expression levels of pro-inflammatory cytokines ( Il1b , Il6 , Tnfα , Ptgs2 ) and anti-inflammatory cytokines ( Il10 , Tgfb ) in gastric tissues. B-E Serum levels of pro-inflammatory (IL-1β, IL-6, TNF-α) and anti-inflammatory (IL-10) cytokines. F, G TUNEL staining and semi-quantitative analysis of apoptotic cells (scale bar = 50 μm). H, I Western blot analysis of cytochrome c, Bax/Bcl-2, and cleaved caspase-3 protein expression. ( n = 3–8). # p < 0.05, ## p < 0.01, ### p < 0.001 vs. control group; * p < 0.05, ** p < 0.01, *** p < 0.001 vs. model group

    Journal: Chinese Medicine

    Article Title: Weiyan Tongluo Granules attenuate gastric intestinal metaplasia through PPARγ/NF-κB/CDX2 signaling pathway

    doi: 10.1186/s13020-026-01350-y

    Figure Lengend Snippet: Effects of WYTLG on inflammatory factors and apoptosis in GIM rats. A Relative mRNA expression levels of pro-inflammatory cytokines ( Il1b , Il6 , Tnfα , Ptgs2 ) and anti-inflammatory cytokines ( Il10 , Tgfb ) in gastric tissues. B-E Serum levels of pro-inflammatory (IL-1β, IL-6, TNF-α) and anti-inflammatory (IL-10) cytokines. F, G TUNEL staining and semi-quantitative analysis of apoptotic cells (scale bar = 50 μm). H, I Western blot analysis of cytochrome c, Bax/Bcl-2, and cleaved caspase-3 protein expression. ( n = 3–8). # p < 0.05, ## p < 0.01, ### p < 0.001 vs. control group; * p < 0.05, ** p < 0.01, *** p < 0.001 vs. model group

    Article Snippet: The experimental groups were then treated with varying concentrations of DCA, drug-containing serum, TNF-α (31–45) (MedChemexpress, USA), or GW9662 (MedChemexpress, USA).

    Techniques: Expressing, TUNEL Assay, Staining, Western Blot, Control

    Hyperinflammatory cytokine and IFN responses in patient PBMCs. (A–H) PBMCs from the patient (red) and three controls (grey) were left untreated (UT), stimulated with TLR4 agonist LPS, TLR7/8 agonist R848, transfected with PolyIC for TLR3/MDA5/RIG-I stimulation, or mock transfected (transf ctrl). Cells were harvested 24 h after treatment, and RNA was isolated and analyzed for IFNB1 (B), CXCL10 (C), IL6 (D), and TNF (E) gene transcription by RT-PCR, and cell culture supernatants were collected and analyzed for CXCL10 (F), IL6 (G), and TNF (H) protein by ELISA. Bars indicate mean values ± standard deviation (SD) of a single experiment performed in triplicates. Statistics were calculated using the ordinary One-way ANOVA with Šídák’s multiple comparisons test. * = P < 0.05, ** = P < 0.01, *** = P < 0.001, **** = P < 0.0001, and ns = not significant.

    Journal: Journal of Human Immunity

    Article Title: Viral infection and brain inflammation with seizures in PARK7 deficiency

    doi: 10.70962/jhi.20250044

    Figure Lengend Snippet: Hyperinflammatory cytokine and IFN responses in patient PBMCs. (A–H) PBMCs from the patient (red) and three controls (grey) were left untreated (UT), stimulated with TLR4 agonist LPS, TLR7/8 agonist R848, transfected with PolyIC for TLR3/MDA5/RIG-I stimulation, or mock transfected (transf ctrl). Cells were harvested 24 h after treatment, and RNA was isolated and analyzed for IFNB1 (B), CXCL10 (C), IL6 (D), and TNF (E) gene transcription by RT-PCR, and cell culture supernatants were collected and analyzed for CXCL10 (F), IL6 (G), and TNF (H) protein by ELISA. Bars indicate mean values ± standard deviation (SD) of a single experiment performed in triplicates. Statistics were calculated using the ordinary One-way ANOVA with Šídák’s multiple comparisons test. * = P < 0.05, ** = P < 0.01, *** = P < 0.001, **** = P < 0.0001, and ns = not significant.

    Article Snippet: RT-PCR was performed with the applied Biosystems TaqMan RNA to CT One Step Kit (4392938; Thermo Fisher Scientific) with primers: TBP(Hs00427620_m1), IFNB1(Hs01077958_s1), CXCL10(Hs01124251_g1), TNF(Hs00174128_m1), IL6(Hs00174131_m1), MX1(Hs00895608_m1), and IFNL1(Hs00601677_g1).

    Techniques: Transfection, Isolation, Reverse Transcription Polymerase Chain Reaction, Cell Culture, Enzyme-linked Immunosorbent Assay, Standard Deviation

    Inflammatory cytokine and IFN responses in PBMCs following RSV infection. PBMCs from the patient (P, red) and three controls (C, grey) were mock infected (mock) or infected with RSV (RSV-A strain Long, MOI 1). (A–G) Cells were harvested 24 h after treatment, and RNA was isolated and analyzed for intracellular RSV RNA (A), IFNB1 (B), CXCL10 (C), IL6 (D), and TNF (E) gene expression by RT-PCR. Cell culture supernatants were harvested and analyzed for CXCL10 (F) and TNF (G) protein by ELISA. Bars indicate the mean ± SD values of a single experiment performed in triplicate. Statistics were calculated using the ordinary two-way ANOVA with Šídák’s multiple comparisons. ns = not significant. SD, standard deviation.

    Journal: Journal of Human Immunity

    Article Title: Viral infection and brain inflammation with seizures in PARK7 deficiency

    doi: 10.70962/jhi.20250044

    Figure Lengend Snippet: Inflammatory cytokine and IFN responses in PBMCs following RSV infection. PBMCs from the patient (P, red) and three controls (C, grey) were mock infected (mock) or infected with RSV (RSV-A strain Long, MOI 1). (A–G) Cells were harvested 24 h after treatment, and RNA was isolated and analyzed for intracellular RSV RNA (A), IFNB1 (B), CXCL10 (C), IL6 (D), and TNF (E) gene expression by RT-PCR. Cell culture supernatants were harvested and analyzed for CXCL10 (F) and TNF (G) protein by ELISA. Bars indicate the mean ± SD values of a single experiment performed in triplicate. Statistics were calculated using the ordinary two-way ANOVA with Šídák’s multiple comparisons. ns = not significant. SD, standard deviation.

    Article Snippet: RT-PCR was performed with the applied Biosystems TaqMan RNA to CT One Step Kit (4392938; Thermo Fisher Scientific) with primers: TBP(Hs00427620_m1), IFNB1(Hs01077958_s1), CXCL10(Hs01124251_g1), TNF(Hs00174128_m1), IL6(Hs00174131_m1), MX1(Hs00895608_m1), and IFNL1(Hs00601677_g1).

    Techniques: Infection, Isolation, Gene Expression, Reverse Transcription Polymerase Chain Reaction, Cell Culture, Enzyme-linked Immunosorbent Assay, Standard Deviation

    Generation of PARK7-deficient A549 and SH-SY5Y cells and cytokine responses to RSV infection. (A and B) Immunoblot and RT-PCR demonstrating absence of RSV replication in primary fibroblasts. Primary fibroblasts from a healthy donor were infected with RSV (RSV-A strain Long, MOI 1), and cells were collected at indicated time points. Whole cell lysates were analyzed by immunoblotting for expression of RSV matrix protein (RSV-M2) and compared to vinculin (VCL) as loading control (A), and cells were collected for RNA extraction and quantification of RSV RNA by RT-PCR (B). (C and D) Immunoblot demonstrating KO of PARK7 in A549 pulmonary cells (C) and PARK7 KO in neuronal SH-SY5Y cells (D). Vinculin (VCL, C) and GAPDH (D) were used as loading control. (E) Repeat of experiment shown in , showing additional replicates of two experiments performed in duplicate of human pulmonary A594 cells deficient in PARK7 (red) and control AAVS1 KO (grey) mock treated or infected with RSV (RSV-A strain Long, MOI 1) for 24 and 48 h, and cells were collected for RNA isolation and analysis of RSV RNA by RT-PCR. (F–M) PARK7 KO (red) and control AAVS1 KO (grey) A549 cells were mock treated or infected with RSV (RSV-A, strain Long, MOI 1) for 24 h. (F–I) Cells were collected for RNA isolation, and quantification of IFNL1 (F), CXCL10 (G), IL6 (H), and TNF (I) gene transcription was performed by RT-PCR. (J–M) Cell culture supernatants were collected for IFNλ1 (J), CXLC10 (K), IL6 (L), and TNF (M) protein quantification by ELISA. (N–U) Repeats of experiment shown in , showing an additional two repeat experiments performed in triplicate (N–Q shows the second experiment and R–U shows the third experiment) where neuronal SH-SY5Y cells deficient in PARK7 or control AAVS1 KO were mock transfected (transf ctrl) or transfected with PolyIC (500 ng/ml). Cells were collected after 6 h, and RNA was isolated, and IFNB1 (N and R), CXCL10 (O and S), IL6 (P and T), and MX1 (Q and U) gene transcription quantification by RT-qPCR. Bars indicate mean ± SD values. Statistics were calculated using the two-way ANOVA with multiple comparisons. * = P < 0.05, ** = P < 0.01, *** = P < 0.001, and ns = not significant. SD, standard deviation. Source data are available for this figure: .

    Journal: Journal of Human Immunity

    Article Title: Viral infection and brain inflammation with seizures in PARK7 deficiency

    doi: 10.70962/jhi.20250044

    Figure Lengend Snippet: Generation of PARK7-deficient A549 and SH-SY5Y cells and cytokine responses to RSV infection. (A and B) Immunoblot and RT-PCR demonstrating absence of RSV replication in primary fibroblasts. Primary fibroblasts from a healthy donor were infected with RSV (RSV-A strain Long, MOI 1), and cells were collected at indicated time points. Whole cell lysates were analyzed by immunoblotting for expression of RSV matrix protein (RSV-M2) and compared to vinculin (VCL) as loading control (A), and cells were collected for RNA extraction and quantification of RSV RNA by RT-PCR (B). (C and D) Immunoblot demonstrating KO of PARK7 in A549 pulmonary cells (C) and PARK7 KO in neuronal SH-SY5Y cells (D). Vinculin (VCL, C) and GAPDH (D) were used as loading control. (E) Repeat of experiment shown in , showing additional replicates of two experiments performed in duplicate of human pulmonary A594 cells deficient in PARK7 (red) and control AAVS1 KO (grey) mock treated or infected with RSV (RSV-A strain Long, MOI 1) for 24 and 48 h, and cells were collected for RNA isolation and analysis of RSV RNA by RT-PCR. (F–M) PARK7 KO (red) and control AAVS1 KO (grey) A549 cells were mock treated or infected with RSV (RSV-A, strain Long, MOI 1) for 24 h. (F–I) Cells were collected for RNA isolation, and quantification of IFNL1 (F), CXCL10 (G), IL6 (H), and TNF (I) gene transcription was performed by RT-PCR. (J–M) Cell culture supernatants were collected for IFNλ1 (J), CXLC10 (K), IL6 (L), and TNF (M) protein quantification by ELISA. (N–U) Repeats of experiment shown in , showing an additional two repeat experiments performed in triplicate (N–Q shows the second experiment and R–U shows the third experiment) where neuronal SH-SY5Y cells deficient in PARK7 or control AAVS1 KO were mock transfected (transf ctrl) or transfected with PolyIC (500 ng/ml). Cells were collected after 6 h, and RNA was isolated, and IFNB1 (N and R), CXCL10 (O and S), IL6 (P and T), and MX1 (Q and U) gene transcription quantification by RT-qPCR. Bars indicate mean ± SD values. Statistics were calculated using the two-way ANOVA with multiple comparisons. * = P < 0.05, ** = P < 0.01, *** = P < 0.001, and ns = not significant. SD, standard deviation. Source data are available for this figure: .

    Article Snippet: RT-PCR was performed with the applied Biosystems TaqMan RNA to CT One Step Kit (4392938; Thermo Fisher Scientific) with primers: TBP(Hs00427620_m1), IFNB1(Hs01077958_s1), CXCL10(Hs01124251_g1), TNF(Hs00174128_m1), IL6(Hs00174131_m1), MX1(Hs00895608_m1), and IFNL1(Hs00601677_g1).

    Techniques: Infection, Western Blot, Reverse Transcription Polymerase Chain Reaction, Expressing, Control, RNA Extraction, Isolation, Cell Culture, Enzyme-linked Immunosorbent Assay, Transfection, Quantitative RT-PCR, Standard Deviation

    Single-cell transcriptome analysis highlight predominant role of neutrophil-derived TNF signaling in mediating immune-chondrocyte interaction in the APC-exposed condyles. a Circle plot of TNF signaling network. b Bubble plot of the communication probability of all the significant ligand-receptor pairs that contributed to increasing signaling sent from Stage II neutrophils to each cell population in chondrocytes. c Co-immunofluorescence staining of the condyle for Myeloperoxidase (MPO, green) and TNF-α (red), or for CD68 (green) and TNF-α (red). Co-localization of MPO and TNF-α indicates production of TNF-α from neutrophils. Scale bar: 50 μm for the low-power field, 10 μm for the high-power field. d Semi-quantitation of the expression levels of MPO, CD68 and TNF-α. * P < 0.05. ** P < 0.01. *** P < 0.001. **** P < 0.000 1

    Journal: International Journal of Oral Science

    Article Title: Single-cell transcriptional atlas reveals distinct immune-chondrocyte crosstalk mechanisms in temporomandibular joint osteoarthritis induced by different types of occlusal disorder

    doi: 10.1038/s41368-025-00424-1

    Figure Lengend Snippet: Single-cell transcriptome analysis highlight predominant role of neutrophil-derived TNF signaling in mediating immune-chondrocyte interaction in the APC-exposed condyles. a Circle plot of TNF signaling network. b Bubble plot of the communication probability of all the significant ligand-receptor pairs that contributed to increasing signaling sent from Stage II neutrophils to each cell population in chondrocytes. c Co-immunofluorescence staining of the condyle for Myeloperoxidase (MPO, green) and TNF-α (red), or for CD68 (green) and TNF-α (red). Co-localization of MPO and TNF-α indicates production of TNF-α from neutrophils. Scale bar: 50 μm for the low-power field, 10 μm for the high-power field. d Semi-quantitation of the expression levels of MPO, CD68 and TNF-α. * P < 0.05. ** P < 0.01. *** P < 0.001. **** P < 0.000 1

    Article Snippet: For Etanercept administration, the TNF-α inhibitor Etanercept (Medchemexpress LLC, NJ, USA, 5 mg/kg) was applied by intraperitoneal injection (i.p.) every other day from the onset of APC or UAC model. For Navarixin administration, the CXCR2/CXCR1 inhibitor Navarixin (Medchemexpress LLC, 30 mg/kg, i.p.) was administered every other day during the experimental time frame.

    Techniques: Single Cell, Derivative Assay, Immunofluorescence, Staining, Quantitation Assay, Expressing

    Signal-targeted therapeutic effect on TMJOA induced by different occlusal disorders. a Representative Masson staining, Saffron-O and fast green staining showing histological changes of the condyle subjected to the APC model, with or without administration of Etanercept or Navarixin. Scale bar: 50 μm. b Quantitative assessment of the histological changes evaluated by the thickness of cartilage and Modified Markins score. * P < 0.05. c Representative images showing histological changes of the condyle subjected to the UAC model, in the presence or absence of Etanercept or Navarixin treatment. Scale bar: 50 μm. d Statistical analyses of the thickness of cartilage and Modified Markins score. * P < 0.05

    Journal: International Journal of Oral Science

    Article Title: Single-cell transcriptional atlas reveals distinct immune-chondrocyte crosstalk mechanisms in temporomandibular joint osteoarthritis induced by different types of occlusal disorder

    doi: 10.1038/s41368-025-00424-1

    Figure Lengend Snippet: Signal-targeted therapeutic effect on TMJOA induced by different occlusal disorders. a Representative Masson staining, Saffron-O and fast green staining showing histological changes of the condyle subjected to the APC model, with or without administration of Etanercept or Navarixin. Scale bar: 50 μm. b Quantitative assessment of the histological changes evaluated by the thickness of cartilage and Modified Markins score. * P < 0.05. c Representative images showing histological changes of the condyle subjected to the UAC model, in the presence or absence of Etanercept or Navarixin treatment. Scale bar: 50 μm. d Statistical analyses of the thickness of cartilage and Modified Markins score. * P < 0.05

    Article Snippet: For Etanercept administration, the TNF-α inhibitor Etanercept (Medchemexpress LLC, NJ, USA, 5 mg/kg) was applied by intraperitoneal injection (i.p.) every other day from the onset of APC or UAC model. For Navarixin administration, the CXCR2/CXCR1 inhibitor Navarixin (Medchemexpress LLC, 30 mg/kg, i.p.) was administered every other day during the experimental time frame.

    Techniques: Staining, Modification