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Image Search Results
Journal: ImmunoTargets and Therapy
Article Title: Recombinant Antithrombin Alleviated Pulmonary Injury and Inflammation in LPS-Induced ARDS by Inhibiting IL17a/NF-κB Signaling
doi: 10.2147/ITT.S502925
Figure Lengend Snippet: rAT reduced pulmonary inflammation in LPS-induced ARDS model mice. ( A–D ) The levels of inflammatory factors, including IL-6 ( A ), TNF-α ( B ), IL-8 ( C ), and hs-CRP ( D ), were decreased in the serum of the rAT-treated group, as detected by ELISA. ( E ) Immunohistochemical staining for F4/80 revealed that rAT treatment reduced the proportion of macrophages in the lung tissue of LPS-induced ARDS model mice. ( F ) Immunohistochemical staining for MRCI, a marker of M2 macrophages, showed that rAT treatment increased the proportion of M2 macrophages in the lung tissue of LPS-induced ARDS model mice. ( G ) Immunohistochemical staining for Ly6G, a marker of neutrophils, showed that rAT treatment reduced the proportion of neutrophils in the lung tissue of LPS-induced ARDS model mice. All the data are presented as the means ± SDs of three independent experiments. One-way ANOVA, *p < 0.05, **p < 0.01, ***p < 0.001, ns, not significant; scale bar, 50 μm.
Article Snippet: A mouse CXCL15 ELISA Kit (E-EL-M0269) and a
Techniques: Enzyme-linked Immunosorbent Assay, Immunohistochemical staining, Staining, Marker
Journal: ImmunoTargets and Therapy
Article Title: Recombinant Antithrombin Alleviated Pulmonary Injury and Inflammation in LPS-Induced ARDS by Inhibiting IL17a/NF-κB Signaling
doi: 10.2147/ITT.S502925
Figure Lengend Snippet: The efficacy of rAT in mitigating lung injury, suppressing the immune response, and inhibiting the activation of the NF-κB signaling pathway in LPS-induced ARDS mice were diminished by the administration of IL-17a. ( A ) ELISA results demonstrated that the administration of IL17a inhibited the ability of rAT to reduce inflammatory factors, including IL-6, TNF-α, and IL-8, in the serum of LPS-induced ARDS mice. ( B ) The analysis of the wet/dry weight ratio of the lung tissue revealed that the administration of IL17a counteracted the ability of rAT to alleviate pulmonary exudation in LPS-induced ARDS mice. ( C ) The administration of IL17a did not significantly affect the ability of rAT to reduce the number of cells in the BALF of LPS-induced ARDS mice. ( D ) The administration of IL17a attenuated the ability of rAT to reduce the concentrations of proteins in the BALF of LPS-induced ARDS mice. ( E ) Real-time PCR results showed that the administration of IL17a blocked the ability of rAT to downregulate the expression of target genes in the IL17a/NF-κB signaling pathway. ( F ) The protein levels of the NF-κB signaling pathway were assessed by Western blotting, and gray intensity analysis of the blots showed that the administration of IL17a in LPS-induced ARDS mice counteracted the ability of rAT to suppress the phosphorylation of IκBα, IKKα/β, and P65. The data are expressed as the means ± SDs (n=3 in each group). One-way ANOVA, *p < 0.05, **p < 0.01, ***p < 0.001, and ns not significant.
Article Snippet: A mouse CXCL15 ELISA Kit (E-EL-M0269) and a
Techniques: Activation Assay, Enzyme-linked Immunosorbent Assay, Real-time Polymerase Chain Reaction, Expressing, Western Blot, Phospho-proteomics
Journal: Frontiers in Pharmacology
Article Title: Isoforskolin Alleviates AECOPD by Improving Pulmonary Function and Attenuating Inflammation Which Involves Downregulation of Th17/IL-17A and NF-κB/NLRP3
doi: 10.3389/fphar.2021.721273
Figure Lengend Snippet: ISOF decreased proinflammatory cytokines in the lung homogenate of AECOPD model mice. The levels of TNF-α (A) , IL-1β (B) , IL-6 (C) , IL-17A (D) , MCP-1 (E) , MIG (F) , IP-10 (G), and CRP (H) in each group were measured by the Bio-Plex Pro Mouse Cytokine assay or ELISA. Data are expressed as means ± SEM ( n = 6 in each group). # p < 0.05, ## p < 0.01, and ### p < 0.001 vs. control group; * p < 0.05, ** p < 0.01, and *** p < 0.001 vs. model group.
Article Snippet: Mouse CXCL9/MIG ELISA kit, mouse CXCL10/IP-10 ELISA kit, and
Techniques: Cytokine Assay, Enzyme-linked Immunosorbent Assay