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#28678311   2017/07/05 Save this To Up

Regulation of miR-92a on vascular endothelial aging via mediating Nrf2-KEAP1-ARE signal pathway.

Various human aging-related diseases start with vascular aging, in which the aging of vascular endothelium is the first step to cause a structural and functional deficit of vascular endothelium, leading to vascular disorders. MicroRNA (miR) participates in various processes of body development and pathological processes via mediating cell proliferation, differentiation, and apoptosis. A previous study showed the correlation between cardiovascular disease and miR-92a, whose role and mechanism in vascular endothelial aging has not been reported.

1190 related Products with: Regulation of miR-92a on vascular endothelial aging via mediating Nrf2-KEAP1-ARE signal pathway.

Signal Transduction Anti Signal Transduction Anti Signal Transduction Anti Human Endocrine Gland Vas Human Vascular Endothelia Human Vascular Endothelia Hh Signaling Pathway Anta Mouse Vascular Endothelia Mouse Vascular Endothelia Rat Vascular Endothelial Signal Transduction Anti AP-1 Reporter – HEK293

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#28085100   2017/01/13 Save this To Up

Effects of Ambient Fine Particles PM2.5 on Human HaCaT Cells.

The current study was conducted to observe the effects of fine particulate matter (PM2.5) on human keratinocyte cell line (HaCaT) cells. The potential mechanism linking PM2.5 and skin was explored. HaCaT cells were cultured and then accessed in plate with PM2.5. Cell viability was tested by Cell Counting Kit-8. The mRNA and protein expression of Filaggrin, Loricrin, Involucrin, and Repetin were analyzed. The levels of Granulocyte-macrophage Colony Stimulating Factor, Thymic Stromal Lymphopoietin, Tumor Necrosis Factor-α, Interleukin-1α, and Interleukin-8 were detected in the supernatant of the HaCaT cell with enzyme-linked immunosorbent assay kits. Cell viability decreased with the increase in PM2.5. Compared with the control group, the protein expression of Filaggrin, Repetin, Involucrin, and Loricrin showed different expression patterns in PM2.5 treatment groups. The level of Tumor Necrosis Factor-α, Thymic Stromal Lymphopoietin, Interleukin-1α, and Interleukin-8 significantly increased in the cells treated with PM2.5. Ambient PM2.5 may increase the risk of eczema and other skin diseases. The relative mechanism may be associated with the impairment of the skin barrier and the elevation of inflammatory responses.

2072 related Products with: Effects of Ambient Fine Particles PM2.5 on Human HaCaT Cells.

Epidermal Growth Factor ( Epidermal Growth Factor ( Rabbit Anti-Human Red Blo ACTH [D Arg8](4 10)(Human Angiotensin II [Lys0](Hum Anti C Reactive Protein A Anti AGO2 Human, Monoclon Anti AGO2 Human, Monoclon Anti AGO2 Human, Monoclon Anti Human AGO3, Monoclon Epidermal Growth Factor ( Epidermal Growth Factor (

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#27997912   2016/12/20 Save this To Up

Analysis of the Indicating Value of Cardiac Troponin I, Tumor Necrosis Factor-α, Interleukin-18, Mir-1 and Mir-146b for Viral Myocarditis among Children.

The primary objective of this study is to evaluate the diagnosis effect of serum protein factors and microRNAs for children suffering from viral myocarditis (VMC).

1506 related Products with: Analysis of the Indicating Value of Cardiac Troponin I, Tumor Necrosis Factor-α, Interleukin-18, Mir-1 and Mir-146b for Viral Myocarditis among Children.

Human Tumor Necrosis Fact RANK Ligand Soluble, Huma ELISA p55,p60,Pig,Sus scr ELISA Kit for Tumor Necr Growth Differentiation Fa Human Tumor Necrosis Fact TNFRSF1B - Goat polyclona Mouse Tumor Necrosis Fact Recombinant Human Cardiac Recombinant Human Troponi Recombinant Troponin I-C Recombinant Troponin I-C

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#27781339   2016/10/26 Save this To Up

Tumor necrosis factor alpha derived from classically activated "M1" macrophages reduces interstitial cell of Cajal numbers.

Delayed gastric emptying in diabetic mice and humans is associated with changes in macrophage phenotype and loss of interstitial cells of Cajal (ICC) in the gastric muscle layers. In diabetic mice, classically activated M1 macrophages are associated with delayed gastric emptying, whereas alternatively activated M2 macrophages are associated with normal gastric emptying. This study aimed to determine if secreted factors from M1 macrophages could injure mouse ICC in primary culture.

2958 related Products with: Tumor necrosis factor alpha derived from classically activated "M1" macrophages reduces interstitial cell of Cajal numbers.

ELISA Kit for Tumor Necr Human Tumor Necrosis Fact Human Stromal Cell-Derive TNFRSF1B - Goat polyclona Mouse Tumor Necrosis Fact Mouse Stromal Cell-Derive Rat Tumor Necrosis Factor ELISA Kit for Tumor Necro Mouse Tumor Necrosis Fact Human Tumor Necrosis Fact Tumor necrosis factor (TN CELLKINES PLATELET DERIVE

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#27778032   2016/10/25 Save this To Up

Activation of necroptosis in a rat model of acute respiratory distress syndrome induced by oleic acid.

The present study was aimed to investigate the role of necroptosis in the pathogenesis of acute respiratory distress syndrome (ARDS). The rat model of ARDS was induced by intravenous injection of oleic acid (OA), and observed for 4 h. The lung injury was evaluated by arterial blood gas, lung wet-dry weight ratio (W/D) and histological analyses. Simultaneously, bronchoalveolar lavage fluid (BALF) was collected for total and differential cell analysis and total protein determination. Tumor necrosis factor alpha (TNF-α) level in BALF was determined with a rat TNF-α ELISA kit. Expressions of receptor interacting protein kinase 1 (RIPK1), RIPK3 and mixed lineage kinase domain-like protein (MLKL) in lung tissue were determined by Western blot and immunohistochemical staining. The interaction between RIPK1 and RIPK3 was explored by immunoprecipitation. The results showed that, compared with those in control group, total white blood cells count (WBC), polymorphonuclear percentage (PMN%), total protein concentration, TNF-α level in BALF, W/D, and the alveolar-arterial oxygen tension difference (P(A-a)O2) in OA group were significantly increased at 4 h after OA injection. Western blot and immunostaining further showed remarkably increased expressions of RIPK1, RIPK3 and MLKL in lung tissue from OA group. Additionally, immunoprecipitation results indicated an enforced interaction between RIPK1 and RIPK3 in OA group. Collectively, the TNF-α level in BALF and the RIPK1-RIPK3-MLKL signaling pathway in lung tissue were found to be upregulated and activated with the process of ARDS. These findings implicate that RIPK1/RIPK3-mediated necroptosis plays a possible role in the pathogenesis of ARDS, which may provide a new idea to develop novel drugs for the therapy of ARDS.

1459 related Products with: Activation of necroptosis in a rat model of acute respiratory distress syndrome induced by oleic acid.

Rat intestinal fatty acid Anti-AICDA(Activation-ind Anti AICDA(Activation ind Anti AGO2 Human, Monoclon Anti AGO2 Mouse, Monoclon Anti AGO2 Human, Monoclon Anti AGO2 Mouse, Monoclon Goat Anti-Rat MARCH10, (i Goat Anti-Mouse, Rat DLL1 Goat Anti-Human, Mouse, R Goat Anti-Human, Mouse, R Goat Anti-Rat Connexin 43

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#27421015   2016/07/16 Save this To Up

Quercetin ameliorates LPS-induced inflammation in human peripheral blood mononuclear cells by inhibition of the TLR2-NF-κB pathway.

Quercetin, a dietary flavonoid abundant in fruits, vegetables, and herbs, presents various pharmacological effects. This study aimed to investigate the anti-inflammatory effect and the underlying mechanism of quercetin in lipopolysaccharide (LPS)-stimulated human peripheral blood mononuclear cells (PBMCs). Cell viability was measured by the Cell Counting Kit-8 assay. The mRNA expression of Toll-like receptor 2 (TLR2) was assessed by quantitative real-time polymerase chain reaction. Inflammatory cytokine secretions and nuclear factor (NF)-kB levels were analyzed by enzyme-linked immunosorbent assay. Our findings showed that quercetin significantly reduced LPS-induced cytotoxicity in human PBMCs. Quercetin suppressed the secretion of tumor necrosis factor-a, interleukin (IL)-1b, and IL-6 in LPS-stimulated human PBMCs. Moreover, quercetin reduced the LPS-induced increase in the expression of TLR2 mRNA and decreased the NF-kB concentration in LPS-stimulated human PBMCs. The data indicates that quercetin plays an important role in LPS-induced inflammation in human PBMCs via suppression of the TLR2-NF-kB pathway.

2618 related Products with: Quercetin ameliorates LPS-induced inflammation in human peripheral blood mononuclear cells by inhibition of the TLR2-NF-κB pathway.

Anti AGO2 Human, Monoclon Anti AGO2 Human, Monoclon Human Epstein-Barr Virus Macrophage Colony Stimula Macrophage Colony Stimula anti H inh human blood an TGF beta induced factor 2 Anti beta3 AR Human, Poly NF-kB Phospho-Specific Ar NF-kB II Phospho-Specific Inflammation (Human) Anti Inflammation (Human) Anti

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#27381730   2016/07/06 Save this To Up

Cholangiocarcinoma-derived exosomes inhibit the antitumor activity of cytokine-induced killer cells by down-regulating the secretion of tumor necrosis factor-α and perforin.

The aim of our study is to observe the impact of cholangiocarcinoma-derived exosomes on the antitumor activities of cytokine-induced killer (CIK) cells and then demonstrate the appropriate mechanism.

2813 related Products with: Cholangiocarcinoma-derived exosomes inhibit the antitumor activity of cytokine-induced killer cells by down-regulating the secretion of tumor necrosis factor-α and perforin.

ELISA Kit for Tumor Necr Human Tumor Necrosis Fact Human Tumor Necrosis Fact Macrophage Colony Stimula Macrophage Colony Stimula TNFRSF1B - Goat polyclona RANK Ligand Soluble, Huma Mouse Tumor Necrosis Fact Rat Tumor Necrosis Factor ELISA p55,p60,Pig,Sus scr Human Tumor necrosis fact ELISA Kit for Tumor Necro

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#27338335   2016/06/24 Save this To Up

Anti-Inflammatory Effects of Melandrii Herba Ethanol Extract via Inhibition of NF-κB and MAPK Signaling Pathways and Induction of HO-1 in RAW 264.7 Cells and Mouse Primary Macrophages.

Melandrii Herba (MH) is a traditional Asian medicinal herb used to treat breast cancer, anuria, and diseases of lactation. However, its biological properties and molecular mechanisms have not been fully elucidated. The purpose of this study was to investigate the anti-inflammatory activity and underlying molecular mechanism of MH ethanol extract (MHE) on the lipopolysaccharide (LPS)-mediated inflammatory response in macrophages. MHE cytotoxicity was determined using a cell counting kit (CCK) assay. The effects of MHE on the production of NO, inflammatory cytokines, and related proteins and mRNAs were determined using the Griess test, ELISA, Western blotting, and real-time RT-PCR, respectively. In addition, intracellular signaling pathways, such as NF-κB, MAPK, and HO-1, were analyzed using Western blotting. Our results revealed that MHE treatment significantly inhibited the secretion of NO and inflammatory cytokines, including TNF-α, IL-6, and IL-1β in macrophages, at sub-cytotoxic concentrations. Furthermore, MHE treatment inhibited iNOS expression and induced HO-1 expression. Finally, the transcriptional activities of NF-κB and MAPK activation were significantly suppressed by MHE in LPS-stimulated macrophages. The results indicate that MHE exerts anti-inflammatory effects by suppressing inflammatory mediator production via NF-κB and MAPK signaling pathways inhibition and induction of HO-1 expression in macrophages. Therefore, our results suggest the potential value of MHE as an inflammatory therapeutic agent developed from a natural substance.

2285 related Products with: Anti-Inflammatory Effects of Melandrii Herba Ethanol Extract via Inhibition of NF-κB and MAPK Signaling Pathways and Induction of HO-1 in RAW 264.7 Cells and Mouse Primary Macrophages.

Rabbit Anti-Human Androge ∆2-Androstene-1α,17β- Androst-16-en-3-ol C19H30 (5α)-Androst-2-en-17-one (5α)-Androstane-3,11,17- Rabbit Anti-Rat Androgen Goat Anti-Rat Actin-like Mouse Anti-Lipoprotein Li Rat monoclonal anti mouse Rabbit anti Androgen Rece Anti-Androgen Receptor pr Anti Androgen Receptor pr

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#27092422   2016/09/17 Save this To Up

Development of an interleukin (IL)-33 sandwich ELISA kit specific for mature IL-33.

Interleukin (IL)-33 is an inflammatory cytokine and belongs to the IL-1 family of cytokines. There are eleven members of the IL-1 family of cytokines and all have important roles in host defense against infections. Their levels are increased during infection and in various auto-inflammatory diseases. IL-33 is also associated with autoimmune diseases such as asthma, atopic dermatitis, rheumatoid arthritis, and atherosclerosis. IL-33 receptors consist of IL-1R4 and IL-1R3 to induce both Th1 and Th2 type immune response. Here we present the development of monoclonal antibodies (mAbs) against human mature IL-33. Recombinant human mature IL-33 protein was expressed in E. coli and purified by multi-step affinity chromatography. The human IL-33 activity was examined in HMC-1 and Raw 264.7 cells. Mice were immunized with the biologically active mature IL-33 to generate mAb against IL-33. The anti-IL-33 mAb (clone/4) was used as a capture antibody for a sandwich enzyme-linked immunosorbent assay (ELISA). This assay detects mature IL-33 with a high sensitivity (80 pg/mL) but does not recognize the biologically inactive precursor IL-33. This article describes the methods for a newly developed IL-33 ELISA kit that is specific for mature IL-33 and may be used to analyze bioactive mature IL-33 in various immunological diseases.

1524 related Products with: Development of an interleukin (IL)-33 sandwich ELISA kit specific for mature IL-33.

Human interleukin 2(IL-2) Human Interleukin-33 IL-3 Rat Interleukin 1(IL-1)EL Rat Interleukin 13(IL-13) Rat Interleukin 1α(IL-1 Rat Interleukin 2(IL-2)EL Recombinant Mouse Interle Human Interleukin 4,IL-4 Human Interleukin 6,IL-6 Pig interleukin 4,IL-4 EL Horse Interleukin 6(IL-6) Mouse Interleukin-1 (IL-1

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#27003121   2016/05/14 Save this To Up

Generation and characterization of a unique panel of anti-adalimumab specific antibodies and their application in therapeutic drug monitoring assays.

A number of assays are currently available to support therapeutic drug monitoring of adalimumab. A complete characterization of the assays and comparison of different assays has not been performed. The aim of this study, therefore, is to generate and characterize of a panel of monoclonal antibodies towards adalimumab (MA-ADM); to use this panel to develop novel assays to determine adalimumab concentrations; to assess the impact of tumor necrosis factor (TNF) and (non-)neutralizing antibodies on adalimumab detection and to compare the performance of assays. In total, ten specific MA-ADM were generated of which four revealed a neutralizing potency of >78%. At least six different clusters were identified using principal component analysis. MA-ADM40D8 was selected as detecting antibody to determine adalimumab in the TNF-coated ELISA (A) and the MA-ADM28B8/MA-ADM40D8 antibody pair was chosen for use in the MA-coated ELISA (B). The impact of TNF and (non-) neutralizing antibodies was similar in both ELISAs. Finally, serum samples of adalimumab-treated Crohn's disease patients were collected and used for an external validation using the assay of Sanquin (C) and the apDia kit (D). All adalimumab assays showed excellent Pearson correlation: r=0.96 for A versus B, 0.96 for A versus C, 0.94 for A versus D, 0.97 for B versus C, 0.95 for B versus D and 0.94 for C and D. The excellent agreement with the two commercially available ELISAs allows harmonization of treatment algorithms in and between different hospitals/infusion centers.

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Rabbit Anti-Human Androge Goat Anti-Human Androgen Rabbit Anti-Rat Androgen Multiple organ tumor tiss MOUSE ANTI BOVINE ROTAVIR Goat Anti- TRPM8, (intern Goat Anti- TFAP2D, (inter Goat Anti- T1R3, (interna Goat Anti-Human Synaptota Goat Anti-Human STK39 SPA Goat Anti-Human SPHK1, (i Goat Anti-Human SODD, (in

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