In a macrophage-membrane binding assay, EDTA inhibited VIP binding in a dose-dependent manner, with an IC50 of 5.4 mM.
In plain wordsIn lab tests, the root canal chemical EDTA reduced how much VIP bound to immune cell membranes, with more EDTA giving more reduction.
- Outcome
- DecreaseEDTA inhibition of VIP binding to macrophage membranes
- Study
n: not reported in source
Macrophage membrane binding assay with [125I]VIP tracer- Outcome group
- Receptor activity and mechanism · Immune and inflammation
Measurements
- IC50
- 5.4 mM
- EDTA inhibition of VIP binding to macrophage membranes
Source sentences
Results showed that EDTA inhibits VIP binding to MM's in a dose-dependent manner, with an IC50 value of 5.4 mM (p < 0.01).
2 context sentences(design, population, supporting numbers)
The purpose of this study was to investigate the effect of the disodium salt of ethylenediamine tetraacetate (EDTA), a calcium ion chelator used in the root canal therapy, on vasoactive intestinal peptide (VIP) binding to macrophage membranes (MM's).
Binding assays were conducted at 15 degrees C in 0.5 ml of 50 mM Tris-HCl buffer (pH 7.5) containing 1.6% (w/v) bovine serum albumin, 1.2 mg/ml of bacitracin, and different EDTA concentrations, using 45 pM of [125I]VIP as tracer.
In this study, Vasoactive intestinal peptide (VIP, aviptadil) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking Vasoactive intestinal peptide (VIP, aviptadil).