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rat interleukin il 6 antibody  (R&D Systems)


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    R&D Systems rat interleukin il 6 antibody
    Single-cell RNA sequencing (ScRNA-seq) analysis reveals interleukin <t>(IL)-6</t> serves as a key cytokine derived from Kuppfer cells (KCs) in radiation-induced liver disease (RILD). (A) Uniform manifold approximation and projection (UMAP) projection of cells from rat livers in the sham-irradiation (IR) (Ctrl) group and IR group integrated into 30 clusters (n = 3). The cells are colored according to the assigned cluster (middle). (Right) UMAP projection showing cluster composition according to cell origin in the liver. (B) Dot plot depicting integrated Ctrl-IR clusters according to liver cell type-specific marker expression. (C) Relative proportion of each cell subtype in the Ctrl and IR groups as indicated. (D) Relative proportion of each KC cluster in the Ctrl and IR groups as indicated. (E) The top 10 significant characteristic genes of Kupffer_0 are listed. (F) Violin plots showing the expression levels of 3 characteristic genes ( Rsrp1, Rgs1 , and Il6 ) of Kupffer_0 across all major liver cell types in the Ctrl and IR groups. (G) Violin plots depicting the expression of Rsrp1, Rgs1 , and Il6 in distinct KC subtypes. (H) Signaling pathway enrichment in intrahepatic cell-cell interactions between KCs and other intrahepatic cell types (Ctrl vs IR groups in RILD models). NES (red = higher enrichment). Student’s t test; *, P < .05; ⁎⁎ , P < .01; ⁎⁎⁎ , P < .001.
    Rat Interleukin Il 6 Antibody, supplied by R&D Systems, used in various techniques. Bioz Stars score: 94/100, based on 72 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Images

    1) Product Images from "Kupffer Cell-Derived Interleukin-6 Aggravates Radiation-Induced Liver Disease by Activating Hepatocyte STAT3 to Promote Ccng1 Transcription"

    Article Title: Kupffer Cell-Derived Interleukin-6 Aggravates Radiation-Induced Liver Disease by Activating Hepatocyte STAT3 to Promote Ccng1 Transcription

    Journal: Advances in Radiation Oncology

    doi: 10.1016/j.adro.2026.102003

    Single-cell RNA sequencing (ScRNA-seq) analysis reveals interleukin (IL)-6 serves as a key cytokine derived from Kuppfer cells (KCs) in radiation-induced liver disease (RILD). (A) Uniform manifold approximation and projection (UMAP) projection of cells from rat livers in the sham-irradiation (IR) (Ctrl) group and IR group integrated into 30 clusters (n = 3). The cells are colored according to the assigned cluster (middle). (Right) UMAP projection showing cluster composition according to cell origin in the liver. (B) Dot plot depicting integrated Ctrl-IR clusters according to liver cell type-specific marker expression. (C) Relative proportion of each cell subtype in the Ctrl and IR groups as indicated. (D) Relative proportion of each KC cluster in the Ctrl and IR groups as indicated. (E) The top 10 significant characteristic genes of Kupffer_0 are listed. (F) Violin plots showing the expression levels of 3 characteristic genes ( Rsrp1, Rgs1 , and Il6 ) of Kupffer_0 across all major liver cell types in the Ctrl and IR groups. (G) Violin plots depicting the expression of Rsrp1, Rgs1 , and Il6 in distinct KC subtypes. (H) Signaling pathway enrichment in intrahepatic cell-cell interactions between KCs and other intrahepatic cell types (Ctrl vs IR groups in RILD models). NES (red = higher enrichment). Student’s t test; *, P < .05; ⁎⁎ , P < .01; ⁎⁎⁎ , P < .001.
    Figure Legend Snippet: Single-cell RNA sequencing (ScRNA-seq) analysis reveals interleukin (IL)-6 serves as a key cytokine derived from Kuppfer cells (KCs) in radiation-induced liver disease (RILD). (A) Uniform manifold approximation and projection (UMAP) projection of cells from rat livers in the sham-irradiation (IR) (Ctrl) group and IR group integrated into 30 clusters (n = 3). The cells are colored according to the assigned cluster (middle). (Right) UMAP projection showing cluster composition according to cell origin in the liver. (B) Dot plot depicting integrated Ctrl-IR clusters according to liver cell type-specific marker expression. (C) Relative proportion of each cell subtype in the Ctrl and IR groups as indicated. (D) Relative proportion of each KC cluster in the Ctrl and IR groups as indicated. (E) The top 10 significant characteristic genes of Kupffer_0 are listed. (F) Violin plots showing the expression levels of 3 characteristic genes ( Rsrp1, Rgs1 , and Il6 ) of Kupffer_0 across all major liver cell types in the Ctrl and IR groups. (G) Violin plots depicting the expression of Rsrp1, Rgs1 , and Il6 in distinct KC subtypes. (H) Signaling pathway enrichment in intrahepatic cell-cell interactions between KCs and other intrahepatic cell types (Ctrl vs IR groups in RILD models). NES (red = higher enrichment). Student’s t test; *, P < .05; ⁎⁎ , P < .01; ⁎⁎⁎ , P < .001.

    Techniques Used: Single Cell, RNA Sequencing, Derivative Assay, Irradiation, Marker, Expressing

    Blockade of classical IL-6 signaling alleviates radiation-induced liver disease (RILD) in rats. (A) Quantitative enzyme-linked immunosorbent assay (ELISA) analysis of interleukin (IL)-6 protein concentrations in peripheral serum and liver homogenates from Ctrl and irradiation (IR) rats (n = 5). (B) Quantitative ELISA analysis of serum liver enzymes in Ctrl rats or IR rats treated with placebo, anti-IL-6, or sgp130Fc (n = 5). (C) Hematoxylin–eosin (H&E) staining of rat livers. (D) F4/80 staining (red) showing Kupffer cell infiltration in rat livers. (E) Myeloperoxidase (MPO) staining (red) revealed neutrophil infiltration in the rat liver. (F) Costaining of CD31 (red), HNF4α (blue), and TUNEL (green) in rat livers. Student’s t test or analysis of variance (ANOVA); ⁎⁎⁎ , P < .001; ns, nonsignificant.
    Figure Legend Snippet: Blockade of classical IL-6 signaling alleviates radiation-induced liver disease (RILD) in rats. (A) Quantitative enzyme-linked immunosorbent assay (ELISA) analysis of interleukin (IL)-6 protein concentrations in peripheral serum and liver homogenates from Ctrl and irradiation (IR) rats (n = 5). (B) Quantitative ELISA analysis of serum liver enzymes in Ctrl rats or IR rats treated with placebo, anti-IL-6, or sgp130Fc (n = 5). (C) Hematoxylin–eosin (H&E) staining of rat livers. (D) F4/80 staining (red) showing Kupffer cell infiltration in rat livers. (E) Myeloperoxidase (MPO) staining (red) revealed neutrophil infiltration in the rat liver. (F) Costaining of CD31 (red), HNF4α (blue), and TUNEL (green) in rat livers. Student’s t test or analysis of variance (ANOVA); ⁎⁎⁎ , P < .001; ns, nonsignificant.

    Techniques Used: Enzyme-linked Immunosorbent Assay, Irradiation, Staining, TUNEL Assay

    Role of the JAK–STAT signaling pathway in hepatocytes during radiation-induced liver disease (RILD). (A) Volcano plot of differential gene expression analysis in hepatocytes after irradiation (IR). Red and blue indicate upregulated and downregulated genes, respectively. The dotted horizontal line represents a P value of 0.05. The dotted vertical lines represent a log2-fold change of 1.5 or −1.5. (Right) Bubble chart depicting the top 5 Kyoto Encyclopedia of Genes and Genomes (KEGG)-enriched pathways corresponding to down/upregulated genes in hepatocytes after IR (screening the pathways and sorting them from large to small according to the −log 10 P value). (B) Western blot analysis showing p-STAT3 and GAPDH expression in primary hepatocytes isolated from Ctrl rats or IR rats treated with placebo, anti-interleukin (IL)-6, or sgp130Fc (n = 5). (C) Western blot analysis showing p-STAT3 and GAPDH expression in primary hepatocytes isolated from IR rats treated with placebo, ruxolitinib (RUX), or tofacitinib (TOF) (n = 5). (D) Quantitative enzyme-linked immunosorbent assay (ELISA) analysis of serum liver enzymes in IR rats treated with placebo, RUX, or TOF (n = 5). (E) Hematoxylin–eosin (H&E) staining of the livers of IR rats treated with placebo, RUX, or TOF (n = 5). (F) Costaining of HNF4α (red) and TUNEL (green) in the livers of IR rats treated with placebo, RUX, or TOF (n = 5). (G) Overlap of p-STAT3-binding genes identified using ChIP-Seq with upregulated genes ( P < .05 and log2-fold change > 2) in hepatocytes identified using scRNA-seq. (H) Violin plots showing the expression levels of overlapping genes identified using scRNA-seq. (I) qRT‒PCR analysis of overlapping genes in isolated primary hepatocytes from IR rats treated with placebo, RUX, or TOF (n = 5). Analysis of variance (ANOVA); *, P < .05; ⁎⁎ , P < .01; ⁎⁎⁎ , P < .001; ns, nonsignificant.
    Figure Legend Snippet: Role of the JAK–STAT signaling pathway in hepatocytes during radiation-induced liver disease (RILD). (A) Volcano plot of differential gene expression analysis in hepatocytes after irradiation (IR). Red and blue indicate upregulated and downregulated genes, respectively. The dotted horizontal line represents a P value of 0.05. The dotted vertical lines represent a log2-fold change of 1.5 or −1.5. (Right) Bubble chart depicting the top 5 Kyoto Encyclopedia of Genes and Genomes (KEGG)-enriched pathways corresponding to down/upregulated genes in hepatocytes after IR (screening the pathways and sorting them from large to small according to the −log 10 P value). (B) Western blot analysis showing p-STAT3 and GAPDH expression in primary hepatocytes isolated from Ctrl rats or IR rats treated with placebo, anti-interleukin (IL)-6, or sgp130Fc (n = 5). (C) Western blot analysis showing p-STAT3 and GAPDH expression in primary hepatocytes isolated from IR rats treated with placebo, ruxolitinib (RUX), or tofacitinib (TOF) (n = 5). (D) Quantitative enzyme-linked immunosorbent assay (ELISA) analysis of serum liver enzymes in IR rats treated with placebo, RUX, or TOF (n = 5). (E) Hematoxylin–eosin (H&E) staining of the livers of IR rats treated with placebo, RUX, or TOF (n = 5). (F) Costaining of HNF4α (red) and TUNEL (green) in the livers of IR rats treated with placebo, RUX, or TOF (n = 5). (G) Overlap of p-STAT3-binding genes identified using ChIP-Seq with upregulated genes ( P < .05 and log2-fold change > 2) in hepatocytes identified using scRNA-seq. (H) Violin plots showing the expression levels of overlapping genes identified using scRNA-seq. (I) qRT‒PCR analysis of overlapping genes in isolated primary hepatocytes from IR rats treated with placebo, RUX, or TOF (n = 5). Analysis of variance (ANOVA); *, P < .05; ⁎⁎ , P < .01; ⁎⁎⁎ , P < .001; ns, nonsignificant.

    Techniques Used: Gene Expression, Irradiation, Western Blot, Expressing, Isolation, Enzyme-linked Immunosorbent Assay, Staining, TUNEL Assay, Binding Assay, ChIP-sequencing

    Role of CCNG1 in radiation-induced hepatocyte damage. (A) BRL-3A cells were transfected with empty vector or siCcng1, cultured with or without exogenous interleukin (IL)-6, and then irradiated with a single 10-Gy electron beam. Four hours after irradiation (IR), the apoptotic rate and cell cycle distribution were detected using flow cytometry. (B) Western blot analysis showing CCNG1, γH2AX, TP53, and GAPDH in BRL-3A cells in these 4 groups. (C) Changes in γH2AX and GAPDH in BRL-3A cells transfected with empty vector or siCcng1 at various time points after a single 10-Gy electron beam IR. (D) Western blot analysis showing CCNG1, γH2AX, and GAPDH expression in BRL-3A cells transfected with empty vector or siTp53 and cultured with or without exogenous IL-6 4 hours after a single 10-Gy electron beam IR. (E) Western blot analysis showing CCNG1, γH2AX, TP53, and GAPDH expression in primary hepatocytes isolated from IR rats treated with placebo, RUX, or TOF (n = 5). Analysis of variance (ANOVA) or Student’s t test; *, P < .05; ⁎⁎ , P < .01; ⁎⁎⁎ , P < .001; ns, nonsignificant.
    Figure Legend Snippet: Role of CCNG1 in radiation-induced hepatocyte damage. (A) BRL-3A cells were transfected with empty vector or siCcng1, cultured with or without exogenous interleukin (IL)-6, and then irradiated with a single 10-Gy electron beam. Four hours after irradiation (IR), the apoptotic rate and cell cycle distribution were detected using flow cytometry. (B) Western blot analysis showing CCNG1, γH2AX, TP53, and GAPDH in BRL-3A cells in these 4 groups. (C) Changes in γH2AX and GAPDH in BRL-3A cells transfected with empty vector or siCcng1 at various time points after a single 10-Gy electron beam IR. (D) Western blot analysis showing CCNG1, γH2AX, and GAPDH expression in BRL-3A cells transfected with empty vector or siTp53 and cultured with or without exogenous IL-6 4 hours after a single 10-Gy electron beam IR. (E) Western blot analysis showing CCNG1, γH2AX, TP53, and GAPDH expression in primary hepatocytes isolated from IR rats treated with placebo, RUX, or TOF (n = 5). Analysis of variance (ANOVA) or Student’s t test; *, P < .05; ⁎⁎ , P < .01; ⁎⁎⁎ , P < .001; ns, nonsignificant.

    Techniques Used: Transfection, Plasmid Preparation, Cell Culture, Irradiation, Flow Cytometry, Western Blot, Expressing, Isolation

    Schematic of the Kuppfer cell (KC)-hepatocyte crosstalk mechanism in RILD. Irradiation (IR) stimulates KCs to secrete IL-6, which binds to the IL-6R/gp130 complex on hepatocytes to activate JAK; phosphorylated JAK induces STAT3 phosphorylation, and nuclear-translocated p-STAT3 binds to the Ccng1 promoter to promote its transcription; CCNG1 then regulates MDM2 to mediate ubiquitination-dependent TP53 proteolysis, ultimately enhancing hepatocyte apoptosis and driving radiation-induced liver disease (RILD) progression.
    Figure Legend Snippet: Schematic of the Kuppfer cell (KC)-hepatocyte crosstalk mechanism in RILD. Irradiation (IR) stimulates KCs to secrete IL-6, which binds to the IL-6R/gp130 complex on hepatocytes to activate JAK; phosphorylated JAK induces STAT3 phosphorylation, and nuclear-translocated p-STAT3 binds to the Ccng1 promoter to promote its transcription; CCNG1 then regulates MDM2 to mediate ubiquitination-dependent TP53 proteolysis, ultimately enhancing hepatocyte apoptosis and driving radiation-induced liver disease (RILD) progression.

    Techniques Used: Irradiation, Phospho-proteomics, Ubiquitin Proteomics



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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 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

    Prostaglandin dysregulation and inflammatory response in the RPP model (A–C) Uterine PGF 2α (A), PGE 2 (B), and PGF 2α /PGE 2 ratio (C) on days 12 and 24 of RPP modeling ( n = 3). (D) The protein levels of COX-2 in the uterine tissue on days 12 and 24 of RPP modeling ( n = 3). (E–G) The levels of IL-1β (E), IL-6 (F), and TNF-α (G) in the serum on days 12 and 24 of RPP modeling ( n = 3). Data are presented as the mean ± SD; ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, one-way ANOVA.

    Journal: iScience

    Article Title: A pharmacological rat model of recurrent pelvic pain exhibiting hyperalgesia and depression-like behaviors

    doi: 10.1016/j.isci.2026.115059

    Figure Lengend Snippet: Prostaglandin dysregulation and inflammatory response in the RPP model (A–C) Uterine PGF 2α (A), PGE 2 (B), and PGF 2α /PGE 2 ratio (C) on days 12 and 24 of RPP modeling ( n = 3). (D) The protein levels of COX-2 in the uterine tissue on days 12 and 24 of RPP modeling ( n = 3). (E–G) The levels of IL-1β (E), IL-6 (F), and TNF-α (G) in the serum on days 12 and 24 of RPP modeling ( n = 3). Data are presented as the mean ± SD; ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, one-way ANOVA.

    Article Snippet: Rat IL-6 ELISA Kit , Elabscience , Cat# E-EL-R0015.

    Techniques:

    ATF6 plays a protective role in renal ischemia-reperfusion injury (A–B) The levels of serum Cr and BUN in mice. (C–D) The levels of serum IL-6 and TNF-α in mice. (E–F) The representative images and kidney injury assessment score of HE staining of the kidney. Ceapin-A7 (10 μM) is an ATF6 inhibitor, and AA147 (10 μM) is an ATF6 agonist. Data represent mean ± SDs, and statistical analysis was performed using one-way ANOVA. (∗ p < 0.05).

    Journal: iScience

    Article Title: ATF6 ameliorates renal warm ischemia-reperfusion injury through FHL2-mediated NF-κB signaling pathway

    doi: 10.1016/j.isci.2026.115173

    Figure Lengend Snippet: ATF6 plays a protective role in renal ischemia-reperfusion injury (A–B) The levels of serum Cr and BUN in mice. (C–D) The levels of serum IL-6 and TNF-α in mice. (E–F) The representative images and kidney injury assessment score of HE staining of the kidney. Ceapin-A7 (10 μM) is an ATF6 inhibitor, and AA147 (10 μM) is an ATF6 agonist. Data represent mean ± SDs, and statistical analysis was performed using one-way ANOVA. (∗ p < 0.05).

    Article Snippet: IL-6 ELISA kit , Boster , EK0412.

    Techniques: Staining

    ATF6 plays a protective role in renal ischemia-reperfusion injury (A–B) The levels of serum Cr and BUN in mice. (C–D) The levels of serum IL-6 and TNF-α in mice. (E–F) The representative images and kidney injury assessment score of HE staining of the kidney. (G–H) RT-qPCR analysis of TNF-α and IL-6 expression in cultured HK-2 in response to H/R treatment. (I–J) RT-qPCR analysis of IL-6 and TNF-α expression in cultured HK-2 in response to H/R using siATF6. Data represent mean ± SDs, and statistical analysis was performed using one-way ANOVA. (∗ p < 0.05).

    Journal: iScience

    Article Title: ATF6 ameliorates renal warm ischemia-reperfusion injury through FHL2-mediated NF-κB signaling pathway

    doi: 10.1016/j.isci.2026.115173

    Figure Lengend Snippet: ATF6 plays a protective role in renal ischemia-reperfusion injury (A–B) The levels of serum Cr and BUN in mice. (C–D) The levels of serum IL-6 and TNF-α in mice. (E–F) The representative images and kidney injury assessment score of HE staining of the kidney. (G–H) RT-qPCR analysis of TNF-α and IL-6 expression in cultured HK-2 in response to H/R treatment. (I–J) RT-qPCR analysis of IL-6 and TNF-α expression in cultured HK-2 in response to H/R using siATF6. Data represent mean ± SDs, and statistical analysis was performed using one-way ANOVA. (∗ p < 0.05).

    Article Snippet: IL-6 ELISA kit , Boster , EK0412.

    Techniques: Staining, Quantitative RT-PCR, Expressing, Cell Culture

    Single-cell RNA sequencing (ScRNA-seq) analysis reveals interleukin (IL)-6 serves as a key cytokine derived from Kuppfer cells (KCs) in radiation-induced liver disease (RILD). (A) Uniform manifold approximation and projection (UMAP) projection of cells from rat livers in the sham-irradiation (IR) (Ctrl) group and IR group integrated into 30 clusters (n = 3). The cells are colored according to the assigned cluster (middle). (Right) UMAP projection showing cluster composition according to cell origin in the liver. (B) Dot plot depicting integrated Ctrl-IR clusters according to liver cell type-specific marker expression. (C) Relative proportion of each cell subtype in the Ctrl and IR groups as indicated. (D) Relative proportion of each KC cluster in the Ctrl and IR groups as indicated. (E) The top 10 significant characteristic genes of Kupffer_0 are listed. (F) Violin plots showing the expression levels of 3 characteristic genes ( Rsrp1, Rgs1 , and Il6 ) of Kupffer_0 across all major liver cell types in the Ctrl and IR groups. (G) Violin plots depicting the expression of Rsrp1, Rgs1 , and Il6 in distinct KC subtypes. (H) Signaling pathway enrichment in intrahepatic cell-cell interactions between KCs and other intrahepatic cell types (Ctrl vs IR groups in RILD models). NES (red = higher enrichment). Student’s t test; *, P < .05; ⁎⁎ , P < .01; ⁎⁎⁎ , P < .001.

    Journal: Advances in Radiation Oncology

    Article Title: Kupffer Cell-Derived Interleukin-6 Aggravates Radiation-Induced Liver Disease by Activating Hepatocyte STAT3 to Promote Ccng1 Transcription

    doi: 10.1016/j.adro.2026.102003

    Figure Lengend Snippet: Single-cell RNA sequencing (ScRNA-seq) analysis reveals interleukin (IL)-6 serves as a key cytokine derived from Kuppfer cells (KCs) in radiation-induced liver disease (RILD). (A) Uniform manifold approximation and projection (UMAP) projection of cells from rat livers in the sham-irradiation (IR) (Ctrl) group and IR group integrated into 30 clusters (n = 3). The cells are colored according to the assigned cluster (middle). (Right) UMAP projection showing cluster composition according to cell origin in the liver. (B) Dot plot depicting integrated Ctrl-IR clusters according to liver cell type-specific marker expression. (C) Relative proportion of each cell subtype in the Ctrl and IR groups as indicated. (D) Relative proportion of each KC cluster in the Ctrl and IR groups as indicated. (E) The top 10 significant characteristic genes of Kupffer_0 are listed. (F) Violin plots showing the expression levels of 3 characteristic genes ( Rsrp1, Rgs1 , and Il6 ) of Kupffer_0 across all major liver cell types in the Ctrl and IR groups. (G) Violin plots depicting the expression of Rsrp1, Rgs1 , and Il6 in distinct KC subtypes. (H) Signaling pathway enrichment in intrahepatic cell-cell interactions between KCs and other intrahepatic cell types (Ctrl vs IR groups in RILD models). NES (red = higher enrichment). Student’s t test; *, P < .05; ⁎⁎ , P < .01; ⁎⁎⁎ , P < .001.

    Article Snippet: Either a rat interleukin (IL)-6 antibody (anti-IL-6; R&D Systems, #AF506) or soluble rat gp130 Fc chimera protein (sgp130Fc; R&D Systems, #5029-RG-100) was intraperitoneally injected twice weekly at concentrations of 16.7 μg/kg and 0.5 mg/kg, respectively.

    Techniques: Single Cell, RNA Sequencing, Derivative Assay, Irradiation, Marker, Expressing

    Blockade of classical IL-6 signaling alleviates radiation-induced liver disease (RILD) in rats. (A) Quantitative enzyme-linked immunosorbent assay (ELISA) analysis of interleukin (IL)-6 protein concentrations in peripheral serum and liver homogenates from Ctrl and irradiation (IR) rats (n = 5). (B) Quantitative ELISA analysis of serum liver enzymes in Ctrl rats or IR rats treated with placebo, anti-IL-6, or sgp130Fc (n = 5). (C) Hematoxylin–eosin (H&E) staining of rat livers. (D) F4/80 staining (red) showing Kupffer cell infiltration in rat livers. (E) Myeloperoxidase (MPO) staining (red) revealed neutrophil infiltration in the rat liver. (F) Costaining of CD31 (red), HNF4α (blue), and TUNEL (green) in rat livers. Student’s t test or analysis of variance (ANOVA); ⁎⁎⁎ , P < .001; ns, nonsignificant.

    Journal: Advances in Radiation Oncology

    Article Title: Kupffer Cell-Derived Interleukin-6 Aggravates Radiation-Induced Liver Disease by Activating Hepatocyte STAT3 to Promote Ccng1 Transcription

    doi: 10.1016/j.adro.2026.102003

    Figure Lengend Snippet: Blockade of classical IL-6 signaling alleviates radiation-induced liver disease (RILD) in rats. (A) Quantitative enzyme-linked immunosorbent assay (ELISA) analysis of interleukin (IL)-6 protein concentrations in peripheral serum and liver homogenates from Ctrl and irradiation (IR) rats (n = 5). (B) Quantitative ELISA analysis of serum liver enzymes in Ctrl rats or IR rats treated with placebo, anti-IL-6, or sgp130Fc (n = 5). (C) Hematoxylin–eosin (H&E) staining of rat livers. (D) F4/80 staining (red) showing Kupffer cell infiltration in rat livers. (E) Myeloperoxidase (MPO) staining (red) revealed neutrophil infiltration in the rat liver. (F) Costaining of CD31 (red), HNF4α (blue), and TUNEL (green) in rat livers. Student’s t test or analysis of variance (ANOVA); ⁎⁎⁎ , P < .001; ns, nonsignificant.

    Article Snippet: Either a rat interleukin (IL)-6 antibody (anti-IL-6; R&D Systems, #AF506) or soluble rat gp130 Fc chimera protein (sgp130Fc; R&D Systems, #5029-RG-100) was intraperitoneally injected twice weekly at concentrations of 16.7 μg/kg and 0.5 mg/kg, respectively.

    Techniques: Enzyme-linked Immunosorbent Assay, Irradiation, Staining, TUNEL Assay

    Role of the JAK–STAT signaling pathway in hepatocytes during radiation-induced liver disease (RILD). (A) Volcano plot of differential gene expression analysis in hepatocytes after irradiation (IR). Red and blue indicate upregulated and downregulated genes, respectively. The dotted horizontal line represents a P value of 0.05. The dotted vertical lines represent a log2-fold change of 1.5 or −1.5. (Right) Bubble chart depicting the top 5 Kyoto Encyclopedia of Genes and Genomes (KEGG)-enriched pathways corresponding to down/upregulated genes in hepatocytes after IR (screening the pathways and sorting them from large to small according to the −log 10 P value). (B) Western blot analysis showing p-STAT3 and GAPDH expression in primary hepatocytes isolated from Ctrl rats or IR rats treated with placebo, anti-interleukin (IL)-6, or sgp130Fc (n = 5). (C) Western blot analysis showing p-STAT3 and GAPDH expression in primary hepatocytes isolated from IR rats treated with placebo, ruxolitinib (RUX), or tofacitinib (TOF) (n = 5). (D) Quantitative enzyme-linked immunosorbent assay (ELISA) analysis of serum liver enzymes in IR rats treated with placebo, RUX, or TOF (n = 5). (E) Hematoxylin–eosin (H&E) staining of the livers of IR rats treated with placebo, RUX, or TOF (n = 5). (F) Costaining of HNF4α (red) and TUNEL (green) in the livers of IR rats treated with placebo, RUX, or TOF (n = 5). (G) Overlap of p-STAT3-binding genes identified using ChIP-Seq with upregulated genes ( P < .05 and log2-fold change > 2) in hepatocytes identified using scRNA-seq. (H) Violin plots showing the expression levels of overlapping genes identified using scRNA-seq. (I) qRT‒PCR analysis of overlapping genes in isolated primary hepatocytes from IR rats treated with placebo, RUX, or TOF (n = 5). Analysis of variance (ANOVA); *, P < .05; ⁎⁎ , P < .01; ⁎⁎⁎ , P < .001; ns, nonsignificant.

    Journal: Advances in Radiation Oncology

    Article Title: Kupffer Cell-Derived Interleukin-6 Aggravates Radiation-Induced Liver Disease by Activating Hepatocyte STAT3 to Promote Ccng1 Transcription

    doi: 10.1016/j.adro.2026.102003

    Figure Lengend Snippet: Role of the JAK–STAT signaling pathway in hepatocytes during radiation-induced liver disease (RILD). (A) Volcano plot of differential gene expression analysis in hepatocytes after irradiation (IR). Red and blue indicate upregulated and downregulated genes, respectively. The dotted horizontal line represents a P value of 0.05. The dotted vertical lines represent a log2-fold change of 1.5 or −1.5. (Right) Bubble chart depicting the top 5 Kyoto Encyclopedia of Genes and Genomes (KEGG)-enriched pathways corresponding to down/upregulated genes in hepatocytes after IR (screening the pathways and sorting them from large to small according to the −log 10 P value). (B) Western blot analysis showing p-STAT3 and GAPDH expression in primary hepatocytes isolated from Ctrl rats or IR rats treated with placebo, anti-interleukin (IL)-6, or sgp130Fc (n = 5). (C) Western blot analysis showing p-STAT3 and GAPDH expression in primary hepatocytes isolated from IR rats treated with placebo, ruxolitinib (RUX), or tofacitinib (TOF) (n = 5). (D) Quantitative enzyme-linked immunosorbent assay (ELISA) analysis of serum liver enzymes in IR rats treated with placebo, RUX, or TOF (n = 5). (E) Hematoxylin–eosin (H&E) staining of the livers of IR rats treated with placebo, RUX, or TOF (n = 5). (F) Costaining of HNF4α (red) and TUNEL (green) in the livers of IR rats treated with placebo, RUX, or TOF (n = 5). (G) Overlap of p-STAT3-binding genes identified using ChIP-Seq with upregulated genes ( P < .05 and log2-fold change > 2) in hepatocytes identified using scRNA-seq. (H) Violin plots showing the expression levels of overlapping genes identified using scRNA-seq. (I) qRT‒PCR analysis of overlapping genes in isolated primary hepatocytes from IR rats treated with placebo, RUX, or TOF (n = 5). Analysis of variance (ANOVA); *, P < .05; ⁎⁎ , P < .01; ⁎⁎⁎ , P < .001; ns, nonsignificant.

    Article Snippet: Either a rat interleukin (IL)-6 antibody (anti-IL-6; R&D Systems, #AF506) or soluble rat gp130 Fc chimera protein (sgp130Fc; R&D Systems, #5029-RG-100) was intraperitoneally injected twice weekly at concentrations of 16.7 μg/kg and 0.5 mg/kg, respectively.

    Techniques: Gene Expression, Irradiation, Western Blot, Expressing, Isolation, Enzyme-linked Immunosorbent Assay, Staining, TUNEL Assay, Binding Assay, ChIP-sequencing

    Role of CCNG1 in radiation-induced hepatocyte damage. (A) BRL-3A cells were transfected with empty vector or siCcng1, cultured with or without exogenous interleukin (IL)-6, and then irradiated with a single 10-Gy electron beam. Four hours after irradiation (IR), the apoptotic rate and cell cycle distribution were detected using flow cytometry. (B) Western blot analysis showing CCNG1, γH2AX, TP53, and GAPDH in BRL-3A cells in these 4 groups. (C) Changes in γH2AX and GAPDH in BRL-3A cells transfected with empty vector or siCcng1 at various time points after a single 10-Gy electron beam IR. (D) Western blot analysis showing CCNG1, γH2AX, and GAPDH expression in BRL-3A cells transfected with empty vector or siTp53 and cultured with or without exogenous IL-6 4 hours after a single 10-Gy electron beam IR. (E) Western blot analysis showing CCNG1, γH2AX, TP53, and GAPDH expression in primary hepatocytes isolated from IR rats treated with placebo, RUX, or TOF (n = 5). Analysis of variance (ANOVA) or Student’s t test; *, P < .05; ⁎⁎ , P < .01; ⁎⁎⁎ , P < .001; ns, nonsignificant.

    Journal: Advances in Radiation Oncology

    Article Title: Kupffer Cell-Derived Interleukin-6 Aggravates Radiation-Induced Liver Disease by Activating Hepatocyte STAT3 to Promote Ccng1 Transcription

    doi: 10.1016/j.adro.2026.102003

    Figure Lengend Snippet: Role of CCNG1 in radiation-induced hepatocyte damage. (A) BRL-3A cells were transfected with empty vector or siCcng1, cultured with or without exogenous interleukin (IL)-6, and then irradiated with a single 10-Gy electron beam. Four hours after irradiation (IR), the apoptotic rate and cell cycle distribution were detected using flow cytometry. (B) Western blot analysis showing CCNG1, γH2AX, TP53, and GAPDH in BRL-3A cells in these 4 groups. (C) Changes in γH2AX and GAPDH in BRL-3A cells transfected with empty vector or siCcng1 at various time points after a single 10-Gy electron beam IR. (D) Western blot analysis showing CCNG1, γH2AX, and GAPDH expression in BRL-3A cells transfected with empty vector or siTp53 and cultured with or without exogenous IL-6 4 hours after a single 10-Gy electron beam IR. (E) Western blot analysis showing CCNG1, γH2AX, TP53, and GAPDH expression in primary hepatocytes isolated from IR rats treated with placebo, RUX, or TOF (n = 5). Analysis of variance (ANOVA) or Student’s t test; *, P < .05; ⁎⁎ , P < .01; ⁎⁎⁎ , P < .001; ns, nonsignificant.

    Article Snippet: Either a rat interleukin (IL)-6 antibody (anti-IL-6; R&D Systems, #AF506) or soluble rat gp130 Fc chimera protein (sgp130Fc; R&D Systems, #5029-RG-100) was intraperitoneally injected twice weekly at concentrations of 16.7 μg/kg and 0.5 mg/kg, respectively.

    Techniques: Transfection, Plasmid Preparation, Cell Culture, Irradiation, Flow Cytometry, Western Blot, Expressing, Isolation

    Schematic of the Kuppfer cell (KC)-hepatocyte crosstalk mechanism in RILD. Irradiation (IR) stimulates KCs to secrete IL-6, which binds to the IL-6R/gp130 complex on hepatocytes to activate JAK; phosphorylated JAK induces STAT3 phosphorylation, and nuclear-translocated p-STAT3 binds to the Ccng1 promoter to promote its transcription; CCNG1 then regulates MDM2 to mediate ubiquitination-dependent TP53 proteolysis, ultimately enhancing hepatocyte apoptosis and driving radiation-induced liver disease (RILD) progression.

    Journal: Advances in Radiation Oncology

    Article Title: Kupffer Cell-Derived Interleukin-6 Aggravates Radiation-Induced Liver Disease by Activating Hepatocyte STAT3 to Promote Ccng1 Transcription

    doi: 10.1016/j.adro.2026.102003

    Figure Lengend Snippet: Schematic of the Kuppfer cell (KC)-hepatocyte crosstalk mechanism in RILD. Irradiation (IR) stimulates KCs to secrete IL-6, which binds to the IL-6R/gp130 complex on hepatocytes to activate JAK; phosphorylated JAK induces STAT3 phosphorylation, and nuclear-translocated p-STAT3 binds to the Ccng1 promoter to promote its transcription; CCNG1 then regulates MDM2 to mediate ubiquitination-dependent TP53 proteolysis, ultimately enhancing hepatocyte apoptosis and driving radiation-induced liver disease (RILD) progression.

    Article Snippet: Either a rat interleukin (IL)-6 antibody (anti-IL-6; R&D Systems, #AF506) or soluble rat gp130 Fc chimera protein (sgp130Fc; R&D Systems, #5029-RG-100) was intraperitoneally injected twice weekly at concentrations of 16.7 μg/kg and 0.5 mg/kg, respectively.

    Techniques: Irradiation, Phospho-proteomics, Ubiquitin Proteomics