goat anti il22ra antibody  (R&D Systems)

Journal: Redox Biology

Article Title: Fenofibrate attenuates the adverse effects of radiation on endothelial cells through modulation of ROS-NO signalling and inflammation

doi: 10.1016/j.redox.2025.103994

Figure Lengend Snippet: Analysis of cytokines, interleukins and endothelial mesenchymal transition markers. qPCR analysis of inflammation markers 2d (A) and 7d (B), inflammatory regulators 2d (E) and 7d (F) and EndMT markers 2d (G) and 7d (H) were performed in irradiated HCAECs with and without fenofibrate (Feno). The release of different cytokines including GM-CSF, MCP-1 and IL-6 which were quantified using flow cytometry after 2d (C) and 7d (D). The error bars represent the standard deviation (±SD) (Two-way ANOVA, Tukey's multiple comparisons test; ∗ p ≤ 0.05; ∗∗ p ≤ 0.01; ∗∗∗p ≤ 0.001; ∗∗∗∗ p ≤ 0.0001; n = 3).

Article Snippet: Extracellular release of inflammatory cytokines (e.g., M-CSF, Granzyme B, IFN-γ, IL-2, IL-4, IL-6, IL-10, IL-17A, IL-21, MCP-1 (CCL2), Perforin and TNF-α) in cell culture supernatants were quantitatively measured based on a fluorescent bead-based system using MACSPlex Cytokine Kits (#130-125-800; Miltenyi Biotec, Germany) according to the manufacturer's protocol.

Techniques: Irradiation, Flow Cytometry, Standard Deviation

Journal: Redox Biology

Article Title: Fenofibrate attenuates the adverse effects of radiation on endothelial cells through modulation of ROS-NO signalling and inflammation

doi: 10.1016/j.redox.2025.103994

Figure Lengend Snippet: Proposed mechanism of action of fenofibrate in irradiated HCAECs in-vitro . Irradiation reduced NO signalling via inactivation of the PI3K–AKT–eNOS pathway, whereas fenofibrate reactivated this pathway and restored NO production (A). Consistent with this, irradiation increased ROS generation, NOX activity, MDA levels, and 3-NT levels, while fenofibrate mitigated this effect (B). Irradiation also triggered an inflammatory response, which was counteracted by fenofibrate (C). The released cytokines contribute to inflammation, changes in cytoskeleton organisation and initiation of EndMT, and fenofibrate effectively attenuated the processes (D). Alterations in the pathways described above play a crucial role in the remodelling of vascular endothelial cells involved in the initiation and progression of atherosclerosis. Fenofibrate acts to reduce or restore the effects of irradiation on these pathways (E–F). Solid lines indicate correlations validated in this study, while dashed lines indicate unvalidated correlations.

Article Snippet: Extracellular release of inflammatory cytokines (e.g., M-CSF, Granzyme B, IFN-γ, IL-2, IL-4, IL-6, IL-10, IL-17A, IL-21, MCP-1 (CCL2), Perforin and TNF-α) in cell culture supernatants were quantitatively measured based on a fluorescent bead-based system using MACSPlex Cytokine Kits (#130-125-800; Miltenyi Biotec, Germany) according to the manufacturer's protocol.

Techniques: Irradiation, In Vitro, Activity Assay

Journal: NPJ Biofilms and Microbiomes

Article Title: Microbiota-derived indole-3-acetic acid alleviates rumen epithelial barrier dysfunction during the peripartum period through AhR signaling

doi: 10.1038/s41522-025-00898-1

Figure Lengend Snippet: A , B Immunofluorescence images of tight junction (TJ; ZO-1, Occludin, and Claudin-3) and cell proliferation marker (Ki67 and PCNA) expression. C Average fold change heatmap of the fluorescence intensities of TJ and cell proliferation markers. D The heatmap shows the mRNA expression of TJ and cell proliferation markers. E Western blotting analysis of the protein levels of ZO-1, Occludin, and Claudin-3. F Representative IF images of AhR. G Representative IF images and fluorescence intensity analysis of IL-22. H Correlation analysis between AhR and IL-22. I Western blotting analysis of the AhR/IL-22 pathway-related protein levels. J Heatmap of relative AhR/IL-22 pathway-associated gene expression levels. K Chord diagrams. The results are presented as the mean ± SEM ( n = 3). Unpaired Student’s t-tests (two-sided) were performed to determine differences between the groups; * P < 0.05, ** P < 0.01, and *** P < 0.001 indicate significant differences between the CON group and the KET group.

Article Snippet: Primary antibodies against IL-1β (ABClone, A22257), IL-6 (Proteintech, 26404-1-AP), ZO-1, (Proteintech, 21773-1-AP), TNF-α (ABClone, A11534), Occludin (Proteintech, 27260-1-AP), Claudin-3 (ABClone, A2946), AhR (ABClone, A1451), ARNT (ABClone, A19532), CYP1A1 (Bioss, bs-1606R), CYP1B1 (ABClone, A1377), IL-22 (ABClone, A23665), STAT3 (Proteintech, 10253-2-AP), p-STAT3 (ABClone, AP0474), and Reg3g (Affinity, DF6869) were used.

Techniques: Immunofluorescence, Marker, Expressing, Fluorescence, Western Blot, Gene Expression

Journal: NPJ Biofilms and Microbiomes

Article Title: Microbiota-derived indole-3-acetic acid alleviates rumen epithelial barrier dysfunction during the peripartum period through AhR signaling

doi: 10.1038/s41522-025-00898-1

Figure Lengend Snippet: A LPS and IAA at different doses were added to the BRECs. B Identification of BRECs by Cytokeratin 18 (CK18). C A CCK-8 assay was performed to evaluate cell viability following IAA treatment at different doses for 2, 6, and 12 h. D Western blotting analysis was performed to analyze the protein levels of the AhR/IL-22 pathway, proinflammatory cytokines, TJs, and antimicrobial peptides. E Protein abundance analysis. F mRNA expression analysis. G , H Immunofluorescence images and fluorescence intensity analysis of AhR, IL-22, STAT3, ZO-1, Claudin-3, Occludin, Reg3g, and Ki67. The results are presented as the mean ± SEM ( n = 3). One-way ANOVA followed by Fisher’s LSD post hoc test was performed to determine differences between the groups. a–d Values without identical letters are statistically significant ( P < 0.05).

Article Snippet: Primary antibodies against IL-1β (ABClone, A22257), IL-6 (Proteintech, 26404-1-AP), ZO-1, (Proteintech, 21773-1-AP), TNF-α (ABClone, A11534), Occludin (Proteintech, 27260-1-AP), Claudin-3 (ABClone, A2946), AhR (ABClone, A1451), ARNT (ABClone, A19532), CYP1A1 (Bioss, bs-1606R), CYP1B1 (ABClone, A1377), IL-22 (ABClone, A23665), STAT3 (Proteintech, 10253-2-AP), p-STAT3 (ABClone, AP0474), and Reg3g (Affinity, DF6869) were used.

Techniques: CCK-8 Assay, Western Blot, Quantitative Proteomics, Expressing, Immunofluorescence, Fluorescence

Journal: NPJ Biofilms and Microbiomes

Article Title: Microbiota-derived indole-3-acetic acid alleviates rumen epithelial barrier dysfunction during the peripartum period through AhR signaling

doi: 10.1038/s41522-025-00898-1

Figure Lengend Snippet: A Molecular docking of IAA was performed with the ligand-binding domain of the AhR protein, and its binding energy was –6.469 kcal/mol. B Western blotting analysis of the expression of the AhR/IL-22 pathway, proinflammatory cytokines, TJ proteins, and antimicrobial peptide proteins. C Protein abundance analysis was performed. D mRNA expression analysis was performed. E , F Immunofluorescence images were captured, and fluorescence intensity analysis of AhR, IL-22, STAT3, ZO-1, Claudin-3, Occludin, Reg3g, and Ki67 was performed. The results are presented as the mean ± SEM ( n = 3). One-way ANOVA followed by Fisher’s LSD post hoc test was conducted to determine the differences between the groups. a–c Values without identical letters are statistically significant ( P < 0.05).

Article Snippet: Primary antibodies against IL-1β (ABClone, A22257), IL-6 (Proteintech, 26404-1-AP), ZO-1, (Proteintech, 21773-1-AP), TNF-α (ABClone, A11534), Occludin (Proteintech, 27260-1-AP), Claudin-3 (ABClone, A2946), AhR (ABClone, A1451), ARNT (ABClone, A19532), CYP1A1 (Bioss, bs-1606R), CYP1B1 (ABClone, A1377), IL-22 (ABClone, A23665), STAT3 (Proteintech, 10253-2-AP), p-STAT3 (ABClone, AP0474), and Reg3g (Affinity, DF6869) were used.

Techniques: Ligand Binding Assay, Binding Assay, Western Blot, Expressing, Quantitative Proteomics, Immunofluorescence, Fluorescence