Rat Brain Natriuretic Peptide-32 ELISA Kit

Name: Rat Brain Natriuretic Peptide-32 ELISA Kit
SKU: DEIA1758
Rating: 5 (1 reviews)

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

COA

SDS

Datasheet

Summary

Sample

Plasma, Serum

Species Reactivity

Rat

Detection Method

sELISA

Intended Use

This assay employs a quantitative enzyme immunoassay technique that measures the rat Brain Natriuretic Peptide 32 (BNP-32) in samples.

Contents of Kit

1. Rat BNP-32 Microplate: A 96-well polystyrene microplate (12 strips of 8 wells) coated with a polyclonal antibody against rat BNP-32.
2. Sealing Tapes: Each kit contains 3 precut, pressure sensitive sealing tapes that can be cut to fit the format of the individual assay.
3. Rat BNP-32 Standard: Rat BNP-32 in a buffered protein base (10 ng, lyophilized).
4. Biotinylated Rat BNP-32 Antibody (40×): A 40-fold concentrated biotinylated polyclonal antibody against rat BNP-32 (150 μl).
5. MIX Diluent Concentrate (10×): A 10-fold concentrated buffered protein base (30 ml).
6. Wash Buffer Concentrate (20×): A 20-fold concentrated buffered surfactant (30 ml, 2 bottles).
7. SP Conjugate (100×): A 100-fold concentrate (80 μl).
8. Chromogen Substrate (1×): A stabilized peroxidase chromogen substrate tetramethylbenzidine (7 ml).
9. Stop Solution (1×): A 0.5 N hydrochloric acid solution to stop the chromogen substrate reaction (11 ml).

Storage

1. Upon arrival, immediately store components of the kit at recommended temperatures up to the expiration date.
2. Store SP Conjugate and Biotinylated Antibody at -20°C.
3. Store Microplate, Diluent Concentrate (10×), Wash Buffer, Stop Solution, and Chromogen Substrate at 2-8°C.
4. Unused microplate wells may be returned to the foil pouch with the desiccant packs and resealed. May be stored for up to 30 days in a vacuum desiccator.
5. Store Standard at 2-8°C before reconstituting with Diluent and at -20°C after reconstituting with Diluent.

Precision

Intra-Assay Precision CV (%) 4.9%
Inter-Assay Precision CV (%) 10.7%

Detection Limit

The minimum detectable dose of rat BNP-32 as calculated by 2SD from the mean of a zero standard was established to be 18 pg/ml.

General Description

Natriuretic peptides (ANP, BNP, and CNP) comprise a family of structurally related peptides, which are derived from three different genes and share a 17-amino acid internal ring (1). A high level of plasma BNP may have a strong, independent association with increased mortality rates in patients with primary pulmonary hypertension (PPH), congestive heart failure and/or after acute myocardial infarction (2-4).

Standard Curve

The typical data is provided for reference only. Individual laboratory means may vary from the values listed. Variations between laboratories may be caused by technique differences.

Standard Curve: The curve is provided for illustration only. A standard curve should be generated each time the assay is performed.

Citations

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Documents

pdf COA

pdf SDS

pdf Datasheet

QA & Reviews

Customer Reviews

References

Inhibition of cell proliferation and arrest of cell cycle progression by blocking chloride channels in human laryngeal cancer cell line Hep-2

NEOPLASMA

Authors: Yu, W. F.; Zhao, Y. L.; Wang, K.; Dong, M. M.

Abstract

Chloride channel (ClC) is involved in normal physiological processes and pathology of various diseases. Although it is recognized that blockade of ClC inhibits the cell proliferation, it is not well understood the potential function of ClC in laryngeal cancer. In this study, we investigated the effect of the ClC inhibitor on cell proliferation, cell cycle progression in human laryngeal cancer cell line Hep-2, as well as the effect on the phosphorylation levels of ERK1/2 and AKT1. In this study crystal violet method was used to study the effect of the ClC inhibitor, 5-nitro-2-(3-phenylpropylamino) benzoic acid, NPPB, on Hep-2 cell proliferation. The impaction of the inhibitor on the cell cycle distribution was investigated by the flow cytometry (FCM). Western blot was performed to measure the phosphorylation levels of ERK1/2 and AKT1. Our data indicated ClC played an important role in Hep-2 cell proliferation and cell cycle. NPPB inhibited Hep-2 cell proliferation when compared with the controls. Blockade of ClC arrested cell cycle progression and suppressed the phosphorylation of ERK1/2 and AKT1 in Hep-2 cells by inhibition of cell proliferation by ClC inhibitor (NPPB) could be through arresting cell cycle progression, which is probably by suppressing phosphorylation of ERK1/2 and AKT1.

Volume Regulated Anion Channel Currents of Rat Hippocampal Neurons and Their Contribution to Oxygen-and-Glucose Deprivation Induced Neuronal Death

PLOS ONE

Authors: Zhang, Huaqiu; Cao, H. James; Kimelberg, Harold K.; Zhou, Min

Abstract

Volume-regulated anion channels (VRAC) are widely expressed chloride channels that are critical for the cell volume regulation. In the mammalian central nervous system, the physiological expression of neuronal VRAC and its role in cerebral ischemia are issues largely unknown. We show that hypoosmotic medium induce an outwardly rectifying chloride conductance in CA1 pyramidal neurons in rat hippocampal slices. The induced chloride conductance was sensitive to some of the VRAC inhibitors, namely, IAA-94 (300 mu M) and NPPB (100 mu M), but not to tamoxifen (10 mu M). Using oxygen-andglucose deprivation (OGD) to simulate ischemic conditions in slices, VRAC activation appeared after OGD induced anoxic depolarization (AD) that showed a progressive increase in current amplitude over the period of post-OGD reperfusion. The OGD induced VRAC currents were significantly inhibited by inhibitors for glutamate AMPA (30 mu M NBQX) and NMDA (40 mu M AP-5) receptors in the OGD solution, supporting the view that induction of AD requires an excessive Na+-loading via these receptors that in turn to activate neuronal VRAC. In the presence of NPPB and DCPIB in the post-OGD reperfusion solution, the OGD induced CA1 pyramidal neuron death, as measured by TO-PRO-3-I staining, was significantly reduced, although DCPIB did not appear to be an effective neuronal VRAC blocker. Altogether, we show that rat hippocampal pyramidal neurons express functional VRAC, and ischemic conditions can initial neuronal VRAC activation that may contribute to ischemic neuronal damage.