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乙二胺四乙酸二钠盐抑制血管活性肠肽与巨噬细胞膜的结合:牙髓病学意义

The disodium salt of EDTA inhibits the binding of vasoactive intestinal peptide to macrophage membranes: endodontic implications.

作者信息

Segura J J, Calvo J R, Guerrero J M, Sampedro C, Jimenez A, Llamas R

机构信息

Department of Medical Biochemistry, University of Seville, Spain.

出版信息

J Endod. 1996 Jul;22(7):337-40. doi: 10.1016/S0099-2399(96)80213-5.

Abstract

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. 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). EDTA concentrations equal or higher than 100 mM of abolished VIP-MM interaction. Taking into account that the macrophage plays an essential role in inflammatory reactions and the immune response, we conclude that the apical extrusion of EDTA during root canal therapy could modify VIP-macrophage interaction modulating the inflammatory mechanisms involved in periapical lesions.

摘要

本研究的目的是调查根管治疗中使用的钙离子螯合剂乙二胺四乙酸二钠盐(EDTA)对血管活性肠肽(VIP)与巨噬细胞膜(MM)结合的影响。结合试验在15℃下于0.5ml含1.6%(w/v)牛血清白蛋白、1.2mg/ml杆菌肽和不同浓度EDTA的50mM Tris-HCl缓冲液(pH 7.5)中进行,使用45pM的[125I]VIP作为示踪剂。结果显示,EDTA以剂量依赖性方式抑制VIP与MM的结合,IC50值为5.4mM(p<0.01)。EDTA浓度等于或高于100mM时可消除VIP-MM相互作用。考虑到巨噬细胞在炎症反应和免疫应答中起重要作用,我们得出结论,根管治疗期间EDTA的根尖挤出可能会改变VIP-巨噬细胞相互作用,从而调节根尖周病变中涉及的炎症机制。

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