mouse hs crp  (Elabscience Biotechnology)

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: Theranostics

Article Title: Therapeutic effects of a novel electrode for transcranial direct current stimulation in ischemic stroke mice

doi: 10.7150/thno.90779

Figure Lengend Snippet: Verification of potential signaling pathways of the therapeutic effects of the new HD-tDCS application based on transcriptome analysis. (A) Bar charts of gene expressions for Insig1 , Bag5 , Hdac2 , and U2af2 in the peri-infarct region using qPCR. The expression of these genes was significantly altered by HD-tDCS-FN application compared to that with MCAO. (B) Bar charts of the hs-CRP and TRAIL levels in the peri-infarct region using enzyme-linked immunosorbent assays. The level of TRAIL was significantly reduced in both HD-tDCS-FN groups compared with that in the MCAO group. (C) Representative western blots for NMDA-dependent SREBP signaling and related proteins. The pNR2B(ser1303)/NR2B ratio, preSREBP1, and mSREBP1 levels were significantly decreased in the MCAO+tDCS-FN(cA) group compared with those in the MCAO group. (D) Representative western blots for inflammation-related proteins. COX2 expression was markedly decreased in both MCAO+tDCS-FN groups compared with that in the MCAO group, while only the pAKT(Ser473)/AKT ratio decreased in the MCAO+tDCS-FN(cA) group. β-actin was used as the loading control. All samples were derived from the peri-infarct region (n=5/group). Data are presented as means±SEMs. * P <0.05, ** P <0.01, and *** P <0.001 vs. each group using one-way analysis of variance with Tukey's test. MCAO, middle cerebral artery occlusion; tDCS, transcranial direct current stimulation; FN, new needle-conjugated electrode.

Article Snippet: The protein levels of high-sensitivity C-reactive protein (hs-CRP) and tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) in the peri-infarct region were measured using mouse TRAIL (ab253210; Abcam, Cambridge, UK) and mouse hs-CRP ELISA kits (MBS026987; MyBioSource, San Diego, CA, USA).

Techniques: Protein-Protein interactions, Expressing, Western Blot, Control, Derivative Assay