Substance P‐induction of endothelial nitric oxide synthase expression on human endothelial cells: modulation of this neurogenic inflammation by an Avena Rhealba® oatmeal extract

Abstract

During cutaneous inflammatory diseases, the neuro‐immuno‐cutaneous system is impaired. In atopic dermatitis pathology, a perturbation of neuromediators release such as substance P (SP), calcitonin gene‐related peptide (CGRP) and bradykinin (BK) could be in part involved in the neurogenic inflammatory state; both of these peptides identified in human skin are potent inducers of vasodilatation, may induce pruritus and could mediate their effects via nitric oxide (NO). NO, considered as a major intra/intercellular messenger, is generated by NO synthase (NOS) enzymes identified in several cell types in the skin. NO displaying vasodilator properties are constitutively released and can also be synthesized in response to inflammatory mediators such as SP neuropeptide. The aim of the present study was first to determine whether SP, CGRP and BK were able to stimulate NO release from human endothelial cells (HECs); the second objective was to induce neurogenic inflammation on HECs with SP (10–100 pm) and to evaluate the activity of Avena Rhealba® oatmeal – Roasting extract – (0.001–0.005%) on endothelial NOS (eNOS) mRNA expression by RT‐PCR. Avena Rhealba® significantly inhibits endothelial cells substance P‐induced expression of eNOS. Our results demonstrate the regulator properties of Avena Rhealba® with respect to neurogenic inflammatory response showing therefore a real interest of Avena Rhealba® in atopic dermatitis inflammatory pathology.