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 mouse hs-CRP ELISA Kit (E-EL-M0677) were purchased from Elabscience (Wuhan, China).

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 mouse hs-CRP ELISA Kit (E-EL-M0677) were purchased from Elabscience (Wuhan, China).

Techniques: Activation Assay, Enzyme-linked Immunosorbent Assay, Real-time Polymerase Chain Reaction, Expressing, Western Blot, Phospho-proteomics

Journal: International journal of molecular sciences

Article Title: Modulation of the Cardiovascular Risk in Type 1 Diabetic Rats by Endurance Training in Combination with the Prebiotic Xylooligosaccharide.

doi: 10.3390/ijms251810027

Figure Lengend Snippet: Figure 4. Study design. BP—blood pressure, HR—heart rate, MTE—maximum time to ex- haustion, AC—abdominal circumference, T-AOC—total antioxidant capacity, Il-6—interleukin-6, hsCRP—high-sensitive C-reactive protein, NADH + H+—nicotinamide adenine dinucleotide hydride, CoQ—coenzyme Q, LDH—lactate dehydrogenase, SDH—succinate dehydrogenase.

Article Snippet: Serum T-AOC, IL-6 and hsCRP were analyzed on an enzyme-linked immunosorbent assay (ELISA) microplate reader HumanReader.HS, HUMAN (Wiesbaden, Germany) via commercially available kits [Rat Total antioxidant capacity, T-AOC Elisa kit, Nanjing Pars Biochem CO., Ltd., Nanjing, China; Rat IL-6 (Interleukin 6) ELISA Kit, Elabscience Biotechnology Inc., Houston, TX, USA; Rat hsCRP (high-sensitivity, C-Reactive Protein) Elabscience Biotechnology Inc., Houston, TX, USA].

Techniques:

Journal: BioResearch Open Access

Article Title: Allogeneic Transplantation of Periodontal Ligament-Derived Multipotent Mesenchymal Stromal Cell Sheets in Canine Critical-Size Supra-Alveolar Periodontal Defect Model

doi: 10.1089/biores.2015.0043

Figure Lengend Snippet: Evaluation of immunological reaction in response to allogeneic and autologous transplantation of periodontal ligament cell sheets by enzyme-linked immunosorbent assay. (A) Concentrations of serum C-reactive protein (mg/dL). (B) Concentrations of serum cluster of differentiation 30 (pg/mL). (C) Concentrations of serum interferon-γ (pg/mL). (D) Concentrations of serum interleukin-10 (pg/mL). (A–D) There were no significant differences in the concentrations of these inflammatory markers between the allogeneic and autologous groups at any time point. Open and closed circles indicate actual values for the allogeneic and autologous groups, respectively. Open and closed bars indicate averaged values for the allogeneic and autologous groups, respectively.

Article Snippet: Serum C-reactive protein (CRP), serum interleukin-10 (IL-10), serum interferon-γ (IFN-γ), and serum cluster of differentiation 30 (CD30) were determined using commercially available canine-specific enzyme-linked immunosorbent assay (ELISA) kits: CRP canine high-sensitivity ELISA Kit (Helica Biosystems, Santa Ana, CA); Quantikine canine IL-10; canine IFN-γ (R&D Systems); and canine CD30 ELISA Kit (Novateinbiosciences, Cambridge, MA) ( n = 7 or 8 dogs).

Techniques: Transplantation Assay, Enzyme-linked Immunosorbent Assay