Equol Effectively Inhibits Toxic Activity of Human Neutrophils without Influencing Their Viability

0458997 - ÚOCHB 2017 RIV CH eng J - Journal Article
Pažoureková, S. - Lucová, M. - Nosál, R. - Drábiková, K. - Harmatha, Juraj - Šmidrkal, J. - Jančinová, V.
Equol Effectively Inhibits Toxic Activity of Human Neutrophils without Influencing Their Viability.
Pharmacology. Roč. 97, 3/4 (2016), s. 138-145. ISSN 0031-7012. E-ISSN 1423-0313
Institutional support: RVO:61388963
Keywords : neutrophils * equol * chemiluminescence * reactive oxygen species * p40(phox) * apoptosis
Subject RIV: FR - Pharmacology ; Medidal Chemistry
Impact factor: 1.442, year: 2016

Equol (7,4'-dihydroxy-isoflavan, or 4',7-isoflavandiol) is a chroman derivative produced by intestinal bacteria in response to soy isoflavone intake in some, but not in all, humans. Equol shows strong anti-oxidant, anti-estrogenic, anti-cancerous and anti-inflammatory properties. The antioxidative capacity of equol has recently received considerable attention, and it has been used for preventing and treating several diseases. We investigated the effect of equol on human neutrophils, extra- and intracellular formation of oxidants, the phosphorylation of protein regulating NADPH oxidase and its effect on apoptosis. Neutrophils, isolated from blood from healthy subjects, were tested upon activation with various stimulants, proper for reactive oxygen species (ROS) production and treated by equol. Equol has the ability to reduce the toxic action of neutrophils. With increasing concentrations, equol decreased the amount of oxidants produced by neutrophils both extra-and intracellularly. The phosphorylation of p40(phox) (a component of NADPH oxidase, responsible for the assembly of functional oxidase in intracellular membranes) was reduced in the presence of equol. The experiments showed that equol did not change the number of viable, apoptotic or dead neutrophils significantly in all concentrations used. These results indicate the promising effect of equol in the operation of ROS in different mechanisms in the model of inflammation.
Permanent Link: http://hdl.handle.net/11104/0259194