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Kamiya mouse high-sensitive crp elisa kit
Bcl-2 expression in monocytes results in reduced inflammatory cells infiltration in the hearts of MCP mice. (A) Representative photomicrographs demonstrating immunohistochemical staining with anti-CD45, -Mac-1 and -Mac-3 antibodies in heart sections from 6-month-old wild-type and transgenic mice. Positive-stained cells were visualized with diaminobenzidine (brown). (B–D) Histograms showing the number of CD45-, Mac-1- and Mac-3-positive cells in the hearts of wild-type, MCP and MCP/Bcl-2 mice. *P <0.001 versus wild-type mice; #P <0.05 versus wild-type and MCP mice; n =6 per group per time point. (E) Circulating levels of <t>CRP</t> assayed by <t>ELISA.</t> n =6 per group per time point. *P <0.05 versus wild-type and MCP/Bcl-2 mice; #P <0.05 versus wild-type mice.
Mouse High Sensitive Crp Elisa Kit, supplied by Kamiya, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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1) Product Images from "Monocyte-specific Bcl-2 expression attenuates inflammation and heart failure in monocyte chemoattractant protein-1 (MCP-1)-induced cardiomyopathy "

Article Title: Monocyte-specific Bcl-2 expression attenuates inflammation and heart failure in monocyte chemoattractant protein-1 (MCP-1)-induced cardiomyopathy

Journal:

doi: 10.1016/j.cardiores.2006.03.008

Bcl-2 expression in monocytes results in reduced inflammatory cells infiltration in the hearts of MCP mice. (A) Representative photomicrographs demonstrating immunohistochemical staining with anti-CD45, -Mac-1 and -Mac-3 antibodies in heart sections from 6-month-old wild-type and transgenic mice. Positive-stained cells were visualized with diaminobenzidine (brown). (B–D) Histograms showing the number of CD45-, Mac-1- and Mac-3-positive cells in the hearts of wild-type, MCP and MCP/Bcl-2 mice. *P <0.001 versus wild-type mice; #P <0.05 versus wild-type and MCP mice; n =6 per group per time point. (E) Circulating levels of CRP assayed by ELISA. n =6 per group per time point. *P <0.05 versus wild-type and MCP/Bcl-2 mice; #P <0.05 versus wild-type mice.
Figure Legend Snippet: Bcl-2 expression in monocytes results in reduced inflammatory cells infiltration in the hearts of MCP mice. (A) Representative photomicrographs demonstrating immunohistochemical staining with anti-CD45, -Mac-1 and -Mac-3 antibodies in heart sections from 6-month-old wild-type and transgenic mice. Positive-stained cells were visualized with diaminobenzidine (brown). (B–D) Histograms showing the number of CD45-, Mac-1- and Mac-3-positive cells in the hearts of wild-type, MCP and MCP/Bcl-2 mice. *P <0.001 versus wild-type mice; #P <0.05 versus wild-type and MCP mice; n =6 per group per time point. (E) Circulating levels of CRP assayed by ELISA. n =6 per group per time point. *P <0.05 versus wild-type and MCP/Bcl-2 mice; #P <0.05 versus wild-type mice.

Techniques Used: Expressing, Immunohistochemical staining, Staining, Transgenic Assay, Enzyme-linked Immunosorbent Assay



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Bcl-2 expression in monocytes results in reduced inflammatory cells infiltration in the hearts of MCP mice. (A) Representative photomicrographs demonstrating immunohistochemical staining with anti-CD45, -Mac-1 and -Mac-3 antibodies in heart sections from 6-month-old wild-type and transgenic mice. Positive-stained cells were visualized with diaminobenzidine (brown). (B–D) Histograms showing the number of CD45-, Mac-1- and Mac-3-positive cells in the hearts of wild-type, MCP and MCP/Bcl-2 mice. *P <0.001 versus wild-type mice; #P <0.05 versus wild-type and MCP mice; n =6 per group per time point. (E) Circulating levels of <t>CRP</t> assayed by <t>ELISA.</t> n =6 per group per time point. *P <0.05 versus wild-type and MCP/Bcl-2 mice; #P <0.05 versus wild-type mice.
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Image Search Results


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.

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

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.

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

Bcl-2 expression in monocytes results in reduced inflammatory cells infiltration in the hearts of MCP mice. (A) Representative photomicrographs demonstrating immunohistochemical staining with anti-CD45, -Mac-1 and -Mac-3 antibodies in heart sections from 6-month-old wild-type and transgenic mice. Positive-stained cells were visualized with diaminobenzidine (brown). (B–D) Histograms showing the number of CD45-, Mac-1- and Mac-3-positive cells in the hearts of wild-type, MCP and MCP/Bcl-2 mice. *P <0.001 versus wild-type mice; #P <0.05 versus wild-type and MCP mice; n =6 per group per time point. (E) Circulating levels of CRP assayed by ELISA. n =6 per group per time point. *P <0.05 versus wild-type and MCP/Bcl-2 mice; #P <0.05 versus wild-type mice.

Journal:

Article Title: Monocyte-specific Bcl-2 expression attenuates inflammation and heart failure in monocyte chemoattractant protein-1 (MCP-1)-induced cardiomyopathy

doi: 10.1016/j.cardiores.2006.03.008

Figure Lengend Snippet: Bcl-2 expression in monocytes results in reduced inflammatory cells infiltration in the hearts of MCP mice. (A) Representative photomicrographs demonstrating immunohistochemical staining with anti-CD45, -Mac-1 and -Mac-3 antibodies in heart sections from 6-month-old wild-type and transgenic mice. Positive-stained cells were visualized with diaminobenzidine (brown). (B–D) Histograms showing the number of CD45-, Mac-1- and Mac-3-positive cells in the hearts of wild-type, MCP and MCP/Bcl-2 mice. *P <0.001 versus wild-type mice; #P <0.05 versus wild-type and MCP mice; n =6 per group per time point. (E) Circulating levels of CRP assayed by ELISA. n =6 per group per time point. *P <0.05 versus wild-type and MCP/Bcl-2 mice; #P <0.05 versus wild-type mice.

Article Snippet: The circulating levels of circulating C-reactive protein (CRP) in plasma were measured with mouse high-sensitive CRP ELISA kit (Kamiya Biomedical Company, Seattle, WA), which specifically detects mouse CRP.

Techniques: Expressing, Immunohistochemical staining, Staining, Transgenic Assay, Enzyme-linked Immunosorbent Assay