title: Vascular endothelial cells and dysfunctions: role of melatonin.
abstract: Several pathological conditions, including hypertension, atherosclerosis, diabetes, ischemia/reperfusion injury and nicotine-induced vasculopathy, are associated with vascular endothelial dysfunction characterized by altered secretory output of endothelial cells. Therefore there is a search for molecules and interventions that could restore endothelial function, in particular augmenting NO production, reducing the generation of free radicals and vasoconstrictors and preventing undesired inflammation. The pineal hormone melatonin exhibits several endothelium protective properties: it scavenges free radicals, activates antioxidant defence enzymes, normalizes lipid and blood pressure profile and increases NO bioavailability. Melatonin improved vascular function in experimental hypertension, reducing intimal infiltration and restoring NO production. Melatonin improved the NO pathway also in animal models for the study of diabetes and prevented NO down-regulation and adhesive molecules up-regulation in nicotine-induced vasculopathy. The protection against endothelial damage, vasoconstriction, platelet aggregation and leukocyte infiltration might contribute to the beneficial effects against ischemia-reperfusion injury by melatonin. Therefore, melatonin administration has endothelium-protective potential in several pathological conditions. Nevertheless, it still needs to be established, whether melatonin is able to revert already established endothelial dysfunction in these conditions.
authors.affiliation: Section of Human Anatomy, Department of Biomedical Sciences and Biotechnologies, Viale Europa 11, 25124 Brescia, Italy.
authors.forename: Luigi Fabrizio
authors.initials: LF
authors.lastname: Rodella
authors.forename: Gaia
authors.initials: G
authors.lastname: Favero
authors.forename: Eleonora
authors.initials: E
authors.lastname: Foglio
authors.forename: Claudia
authors.initials: C
authors.lastname: Rossini
authors.forename: Stefania
authors.initials: S
authors.lastname: Castrezzati
authors.forename: Claudio
authors.initials: C
authors.lastname: Lonati
authors.forename: Rita
authors.initials: R
authors.lastname: Rezzani
mesh_terms: D050197:Atherosclerosis / Q000378:metabolism / Q000503:physiopathology*; D003920:Diabetes Mellitus / Q000378:metabolism / Q000503:physiopathology*; D042783:Endothelial Cells / Q000378:metabolism*; D006801:Humans; D006973:Hypertension / Q000378:metabolism*; D008550:Melatonin / Q000378:metabolism*; D009538:Nicotine / Q000633:toxicity; D015427:Reperfusion Injury / Q000378:metabolism*; D014652:Vascular Diseases / Q000139:chemically induced / Q000503:physiopathology*
chemical_list: D009538:Nicotine; D008550:Melatonin