il 6 antibody  (Proteintech)

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

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

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

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

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

Journal: International Dental Journal

Article Title: NLRP12 Alleviated Periodontal Destruction via Suppressing Nuclear Factor Kappa-B Signalling Pathway

doi: 10.1016/j.identj.2026.109417

Figure Lengend Snippet: LPS triggered an inflammatory response and suppressed the osteogenic differentiation potential of PDLSCs. (A) The proliferative capacity of PDLSCs exposed to varying LPS concentrations over 2, 4, and 6 days was measured with CCK-8 assay. (B) The qRT-PCR analysis revealed elevated mRNA expression of inflammatory mediators IL-6, IL-8 , and IL-10 in PDLSCs following treatment with 10 µg/mL LPS. The qRT-PCR (C) and WB (D) analysis revealed significantly lower expression of osteogenic markers (COL1 and RUNX2) in PDLSCs exposed to 10 µg/mL LPS. The ALP (E) and alizarin red (F) staining assays showed that 10 µg/mL LPS significantly inhibited the osteogenic differentiation capacity of PDLSCs compared to the control group. Data were presented as mean ± SD ( n = 3). *** P < .001, **** P < .0001.

Article Snippet: After blocking with 10% normal goat serum (Beyotime), sections were covered overnight at 4°C with primary antibodies against IL-6 (#21865-1-AP; Proteintech), IL-8 (#94407; CST), IL-10 (#ab290735; Abcam), COL1 (#12256; CST) and RUNX2 (#8486; CST), then covered with secondary antibodies Goat Anti-Rabbit IgG (Zsbio), and then stained with DAB (Zsbio) for 20 to 60 seconds and counterstained with haematoxylin.

Techniques: CCK-8 Assay, Quantitative RT-PCR, Expressing, Staining, Control

Journal: International Dental Journal

Article Title: NLRP12 Alleviated Periodontal Destruction via Suppressing Nuclear Factor Kappa-B Signalling Pathway

doi: 10.1016/j.identj.2026.109417

Figure Lengend Snippet: NLRP12 overexpression reduced LPS-induced inflammatory response and reversed LPS-induced suppression of osteogenic differentiation in PDLSCs. (A and B) The qRT-PCR and WB data revealed that expression level of NLRP12 in oeNLRP12 group was increased significantly compared to oeNC group. (C) The qRT-PCR data revealed that mRNA expression of IL-6 and IL-8 was suppressed, while the mRNA expression of IL-10 was increased in oeNLRP12 + LPS group compared to oeNC + LPS group. (D) The expression of COL1 and RUNX2 was increased significantly detected by WB assays in oeNLRP12 + LPS group compared to oeNC + LPS group. (E) Representative pictures of ALP staining showed lower staining in oeNC + LPS group compared to oeNC group and higher staining in oeNLRP12 + LPS group compared to oeNC + LPS group (scale bar = 500 μm). (F) Representative pictures of alizarin red staining showed fewer mineralized nodules in oeNC + LPS group compared to oeNC group and more mineralized nodules in oeNLRP12 + LPS group compared to oeNC + LPS group (scale bar = 500 μm). oeNC: PDLSCs transfected via negative control lentiviral. oeNLRP12: PDLSCs transfected via lentiviral with overexpression- NLRP12 . oeNC + LPS: PDLSCs transfected via negative control lentiviral and subsequently cultured under 10 µg/mL LPS induction. oeNLRP12 + LPS: PDLSCs transfected via lentiviral with overexpression- NLRP12 and subsequently cultured under 10 µg/mL LPS induction. Data were presented as mean ± SD ( n = 3). ns, no significant difference, *** P < .001, **** P < .0001.

Article Snippet: After blocking with 10% normal goat serum (Beyotime), sections were covered overnight at 4°C with primary antibodies against IL-6 (#21865-1-AP; Proteintech), IL-8 (#94407; CST), IL-10 (#ab290735; Abcam), COL1 (#12256; CST) and RUNX2 (#8486; CST), then covered with secondary antibodies Goat Anti-Rabbit IgG (Zsbio), and then stained with DAB (Zsbio) for 20 to 60 seconds and counterstained with haematoxylin.

Techniques: Over Expression, Quantitative RT-PCR, Expressing, Staining, Transfection, Negative Control, Cell Culture

Journal: International Dental Journal

Article Title: NLRP12 Alleviated Periodontal Destruction via Suppressing Nuclear Factor Kappa-B Signalling Pathway

doi: 10.1016/j.identj.2026.109417

Figure Lengend Snippet: Overexpression of NLRP12 alleviated the inflammatory responses and osteogenic differentiation inhibition of PDLSCs by suppressing the NF-κB pathway. (A) WB results showing the changes of protein expression levels of p-p65, p65, p-IκBα, and IκBα in PDLSCs after NLRP12 overexpression. (B) WB results showing the changes of protein expression levels of p-p65 and p65 in PDLSCs overexpressing NLRP12 after PMA treatment. (C)The qRT-PCR results demonstrating the transcriptional expression levels of IL-6, IL-8 , and IL-10 in PDLSCs overexpressing NLRP12 after PMA treatment. (D)WB results demonstrating alterations in the protein expression levels of COL1 and RUNX2 in PDLSCs overexpressing NLRP12 after PMA treatment. (E) Representative pictures showing ALP staining (scale bar = 500 μm) (F) Representative pictures showing alizarin red staining (scale bar = 500 μm). oeNC: PDLSCs transfected via negative control lentiviral. oeNLRP12: PDLSCs transfected via lentiviral with overexpression- NLRP12 . oeNC + LPS: PDLSCs transfected via negative control lentiviral and subsequently cultured under 10 µg/mL LPS. oeNLRP12 + LPS: PDLSCs transfected via lentiviral with overexpression- NLRP12 and subsequently cultured under 10 µg/mL LPS. Data were presented as mean ± SD ( n = 3). ns, no significant difference, * P < .05, ** P < .01, *** P < .001, **** P < .0001.

Article Snippet: After blocking with 10% normal goat serum (Beyotime), sections were covered overnight at 4°C with primary antibodies against IL-6 (#21865-1-AP; Proteintech), IL-8 (#94407; CST), IL-10 (#ab290735; Abcam), COL1 (#12256; CST) and RUNX2 (#8486; CST), then covered with secondary antibodies Goat Anti-Rabbit IgG (Zsbio), and then stained with DAB (Zsbio) for 20 to 60 seconds and counterstained with haematoxylin.

Techniques: Over Expression, Inhibition, Expressing, Quantitative RT-PCR, Staining, Transfection, Negative Control, Cell Culture

Journal: International Dental Journal

Article Title: NLRP12 Alleviated Periodontal Destruction via Suppressing Nuclear Factor Kappa-B Signalling Pathway

doi: 10.1016/j.identj.2026.109417

Figure Lengend Snippet: Overexpression of NLRP12 in PDLSCs alleviated the inflammatory responses and promoted periodontal regeneration in periodontitis rats. (A) The timeline demonstrated the experimental procedures. (B) The micro-CT scanning results. (C) Representative images of H&E staining (the black scale bars and white scale bars are 200 and 100 μm, respectively). (D) Representative images of Masson trichrome staining (the black scale bars and white scale bars are 200 and 100 μm, respectively). (E) Cementoenamel junction (CEJ)–alveolar bone crest (ABC) distance. (F) bone volume/total volume (BV/TV). (G) Loss of attachment in H&E staining. (H) Semiquantitative analysis of Masson trichrome staining. (I) Representative immunohistochemical images showing the expression level of inflammatory factor IL-6, IL-8, and IL-10, osteogenic factor COL1, and RUNX2, and TRAP staining showing the number of osteoclasts. Scale bar = 100 μm. (J) Quantitative analysis of IL-6-positive cells, IL-8-positive cells, IL-10-positive cells, COL1-positive cells, and RUNX2-positive cells. (K) Quantitative result of TRAP+ cells. Control group: without treatment. Periodontitis group: ligature-induced experimental periodontitis model. oeNC group: periodontitis group treated with oeNC PDLSCs. oeNLRP12 group: periodontitis group treated with oeNLRP12 PDLSCs. IHC: immunohistochemistry. IOD, integrated option density. The data are presented as mean ± SD ( n = 6 rats per group). *P < .1 , **P < .01 , ***P < .001 , ****P < .0001 .

Article Snippet: After blocking with 10% normal goat serum (Beyotime), sections were covered overnight at 4°C with primary antibodies against IL-6 (#21865-1-AP; Proteintech), IL-8 (#94407; CST), IL-10 (#ab290735; Abcam), COL1 (#12256; CST) and RUNX2 (#8486; CST), then covered with secondary antibodies Goat Anti-Rabbit IgG (Zsbio), and then stained with DAB (Zsbio) for 20 to 60 seconds and counterstained with haematoxylin.

Techniques: Over Expression, Micro-CT, Staining, Immunohistochemical staining, Expressing, Control, Immunohistochemistry