Mouse Tumor Necrosis Factor Alpha ELISA Kit

Name: Mouse Tumor Necrosis Factor Alpha ELISA Kit
SKU: DEIA7391
Rating: 5 (1 reviews)

Regulatory status: For research use only, not for use in diagnostic procedures.

COA

SDS

Datasheet

Summary

Sample

Serum, plasma, tissue homogenates and other biological fluids

Species Reactivity

Mouse

Detection Method

sELISA

Intended Use

TNF-α ELISA Kit allows for the in vitro quantitative determination of TNF-α concentrations in serum, plasma, tissue homogenates and other biological fluids.

Contents of Kit

Storage

2-8 °C for 6 months

Precision

Intra-assay:CV<8%;
Inter-assay:CV<10%

Detection Range

3.906-250pg/ml

Sensitivity

< 2.344pg/ml

Standard Curve

Citations

Have you cited DEIA7391 in a publication? Let us know and earn a reward for your research.

miR-130b participates in wear particle-induced inflammation and osteolysis via FOXF2/NF-κB pathway

Zheng DZ, Bu YM, Wang L

Immunopharmacol Immunotoxicol2018 OctPubMed ID: 30488739Read Article

Applications: ELISA
Reactive species: Mouse
"Abstract: Objective:To reveal other miR-130b-mediated signaling pathway in the involvement of wear particle-induced inflammation and osteolysis. Materials and methods:Particle-induced osteolysis (PIO) mice model was established. Secretion levels of TNF-α, IL-1β, IL-6, and IL-10 were measured by ELISA. miR-130b and forkhead box F2 (FOXF2) mRNA were detected by qRT-PCR. Protein levels of FOXF2, phosphorylation-p65 (p-p65), and p-IκB were observed by Western blot. Luciferase reporter assay was performed to confirm the regulation of miR-130b on FOXF2."
Article snippet: The protein expressions of TNF-a, IL-1b, IL-6, and IL-10 in PIO periosteum tissues and Raw264.7 cells were quantified by Mouse TNF-a ELISA KIT (Creative Diagnostics, New York, CA, USA), Mouse IL-1b ELISA KIT (Creative Diagnostics), Mouse IL-6 ELISA KIT (*), and Mouse IL-10 ELISA KIT (*) according to the manufacturer’s instructions.

Secretion level of TNF-α in Co-Cr-Mo treated Raw264.7 cells was significantly higher than that of the control group. (Zheng, D.Z., Bu, Y.M. and Wang, L., 2018)

Figure 1. miR-130b, FOXF2, and p-p65 expressions in Raw264.7 cell polarization. Raw264.7 cells were divided into two groups: control group and Co-Cr-Mo group. Secretion level of TNF-α was measured by ELISA.

Secretion level of TNF-α in Raw264.7 cells was significantly upregulated after treated with Co-Cr-Mo. (Zheng, <i>et al</i>, 2018)

Figure 2. miR-130b participated in osteolysis M1 macrophages polarization. M1 macrophages were divided into four groups: control group, Co-Cr-Mo group, CoCr-Mo þ NC group, and Co-Cr-Mo þ miR-130b inhibitor group. Secretion level of TNF-α was measured by ELISA.

Co-Cr-Mo significantly increased secretion levels of IL-1β, miR-130b inhibitor decreased secretion levels of IL-1β, FOXF2 siRNA increased secretion levels of IL-1β, and BAY 11–7082 further decreased secretion levels of IL-1β. (Zheng, <i>et al</i>, 2018)

Figure 3. miR-130b affected Co-Cr-Mo induced macrophages polarization by inhibiting FOXF2 expression to activate the NF-jB pathway. RAW264.7 cells were divided into six groups: control group, Co-Cr-Mo group, Co-Cr-Mo þ NC group, Co-Cr-Mo þ miR-130b inhibitor group, Co-Cr-Mo þ miR-130b inhibitor þ FOXF2 siRNA group, and Co-Cr-Mo þ miR-130b inhibitor þ FOXF2 siRNA þ BAY 11–7082 (10 mM) group. Secretion level of TNF-α was measured by ELISA.

Documents

pdf COA

pdf SDS

pdf Datasheet

QA & Reviews

Customer Reviews

References

Serum Krebs von den Lungen-6 levels in psoriatic patients under treatment with biologics

JOURNAL OF DERMATOLOGY

Authors: Iwata, Hiroaki; Haga, Naoya; Sugai, Tatsuro; Fujita, Yasuyuki

Abstract

During biologic treatments, attention should be paid to adverse reactions, particularly infectious diseases. Furthermore, drug-induced interstitial lung disease is also known to be associated with biologic therapies. We retrospectively reviewed serum Krebs von den Lungen-6 (KL-6) levels in psoriatic patients who underwent treatment with seven different biologics. A total of 67 patients who received 80 biologic treatments were evaluated. The 31 anti-tumor necrosis factor (TNF)-alpha treatments consisted of 17 infliximab (IFX) and 14 adalimumab. The 23 anti-interleukin (IL)-23 treatments consisted of 14 ustekinumab and nine guselkumab. The 26 anti-IL-17 treatments consisted of nine secukinumab, six ixekizumab and 11 brodalumab. The IFX showed significantly increased mean serum KL-6 (170.9%), but none of the other treatments showed significant increases. Thirteen of the 17 (75.6%) patients in the IFX and 17 of the 31 (54.8%) patients in the total anti-TNF-alpha group demonstrated at least a 25% increase in serum KL-6. Levels exceeding the cut-off (500 U/mL) were detected in three patients before treatment and in seven patients after treatment. This study showed that anti-IL-17 and anti-IL-23 treatments have no significant impact on serum KL-6 level. In addition to the influence of IFX, a significantly large number of patients in the IFX group had a history of methotrexate administration associated with psoriatic arthritis, which might have influenced the KL-6 level. None of the patients with elevated serum KL-6 showed pulmonary changes by computed tomography and/or X ray.

Geniposide alleviates diabetic nephropathy of mice through AMPK/SIRT1/NF-kappa B pathway

EUROPEAN JOURNAL OF PHARMACOLOGY

Authors: Li, Fengtao; Chen, Yu; Li, Yongjun; Huang, Meizi; Zhao, Wenchang

Abstract

Geniposide (GE) can effectively inhibit diabetic nephropathy (DN), but its mechanism is unclear. The objective of this study was to explore the antidiabetic nephropathy effects of GE both in high fat diet/streptozotocin-induced DN mice and in high glucose-induced podocyte model. Renal function in DN mice was evaluated by levels of serum creatinine (Scr) and blood urea nitrogen (BUN). Renal inflammation was appraised by pro-inflammatory cytokines: Tumor necrosis factor alpha (TNF-alpha), Interleukin 6 (IL-6) and IL-1 beta via ELISA assay. Renal histopathology analysis was conducted via hematoxylin and eosin, Masson and periodic acid-silver metheramine staining. Cellular viability was measured by Terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling assay. Moreover, the related proteins p-NF-kappa B, ASC, Cleave-IL-1 beta, NLRP3, Cleave-Caspase-1 and GSDMD-N in AMPK/SIRT1/NF-kappa B pathway were assayed by Western blotting. In order to further investigate the effects of GE on podocytes, we also assessed these protein levels in AMPK/SIRT1/NF-kappa B pathway after siRNA-AMPK intervention by Western blotting. GE alleviated renal dysfunction as evidenced by decreased levels of Scr, BUN, TNF-alpha, IL-6 and IK-1 beta. Histological examination revealed GE effectively attenuated kidney damage, including glomerular basement membrane thickening and inflammatory cells infiltration. AMPK, p-AMPK and SIRT1 levels were obviously decreased both in DN mice and in podocyte model, but GE reversed these changes. The protein expressions in APMK/SIRT1/NF-kappa B pathway were significantly decreased by GE treatment. These results suggested that GE could efficiently block oxidative stress and inflammatory responses accompanied with pyroptosis, thus inhibiting the development of DN, and its mechanism might be related to APMK/SIRT1/NF-kappa B pathway.