Keywords
Abstract
The manuscript provides an overview of contemporary data dealing with resveratrol action. Resveratrol is trans-3,5,4’-trihydroxystilbene and is contained in grapes, cherries, berries, peanuts, pines, plums, some herbs. Its structure consists of two aromatic rings, connecting by methylene double bonds that is the part of resorcinol, from that resveratrol has obtained its name. Resveratrol is produced in plants by the enzyme stilbene synthase in the case of infections or mechanical damages. Resveratrol is present in cis- and transisomer forms. Trans form of resveratrol is predominant and more stable. There are some special targets to resveratrol. Resveratrol activates sirtuin-1 (SIRT-1). Sirtuins are a family of deacetylase enzymes. Other resveratrol targets include nuclear factor erythroid 2-reductes factor 2 (Nrf2) and factor of transcription nuclear factor kappa B (NFkB), AMP-activated protein kinase (AMPK). Resveratrol acts on NAD content that is connected with phosphodiesterase activity. Resveratrol reduces the oxidative load through suppressing NADPH oxidase mediated production of ROS. Resveratrol suppresses oxidation of human low-density lipoproteins as well as reduces lipid peroxidation. Resveratrol activates antioxidant
enzymes such as superoxide dismutase, glutathione peroxidase, catalase, glutathione-S-transferase in rat myocardium and aorta. One potential cardioprotective mechanism of resveratrol action is the inhibition of low-density lipoproteins oxidation. The beneficial properties of the phenolic compounds in grapes and vine have been extremely studied after the discovery of the phenomena «French Paradox». Vasculoprotective benefits of resveratrol enclose an increase in formation of the vasculoprotective nitric oxide. Such effect was studied in human umbilical vein endothelial cells. Resveratrol induced the expression of endothelial nitric oxide synthase thus leading to an increased NO synthesis. These effects of resveratrol on endothelial cells are fostered by the activation of estrogen receptor and nitrogen-activated protein kinase signaling and additionally mediated by SIRT 1 and the transcription factors FOXO 1 and FOXO 3. The enhancement of eNOS synthesis and NO production was facilitated endothelial cells activity and was connected with interaction with estrogen receptors and peroxisome proliferator-activated receptors α (PPARα). Resveratrol also suppressed the expression of vasculoprotective transcription factor Kruppel-like factor 2 via SIRT1 activation. These alterations were accompanied by diminution of endothelin-1 and increase of NO synthesis and of vascular endothelial growth factor (VECF) in the heart of experimental rats. Vasoprotective effects of resveratrol are connected with anti-inflammatory action that is realized by lipoxygenase, cyclooxigenase-1, cyclooxygenase 2 inhibition. Antihypertensive effects of resveratrol have been observed in several animal models and were connected with increase of endothelial NO production decrease of endothelin-1 synthesis, reduce vascular oxidative stress and prevention of smooth muscles proliferation, vascular remodeling and arterial stiffness. Cardioprotective action of resveratrol is connected with its antioxidant, hypolipidemic, anti-inflammatory action. Resveratrol has low bioavailability that`s why it is recommended in topic drugs for use. In cardiologic
pharmacotherapy the natural complex resverazine consisting of resveratrol is proposed for the treatment of patients with lipid, carbohydrate metabolism disturbances, in the cases of obesity, metabolic syndrome.