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      The Cardiovascular Protective Effects of Chrysin: A Narrative Review on Experimental Researches

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          Abstract

          Chrysin is one of the flavonoids fruits, vegetables, and plant especially found in honey, it has been indicated that its cardiovascular protective effect is due to its antioxidative effects and anti-inflammatory activities. Chrysin exerts an antioxidant effect by enhancing the antioxidant system, suppressing pro-oxidant enzymes, scavenging free radicals and chelating redox active transition-metal ions. Chrysin decreases lipid synthesis and also increases its metabolism, thereby ameliorating blood lipid profile. Chrysin modulates vascular function by increasing the bioavailability of endothelial nitric oxide. Chrysin inhibits the development of atherosclerosis by decreasing vascular inflammation. The anti-inflammatory effects of chrysin may relate to its inhibitory effect on the nuclear transcriptional factor-kB signaling pathway. It also prevents vascular smooth muscle cells proliferation and thrombogenesis. Altogether, chrysin may be effective as a natural agent for the prevention and treatment of cardiovascular diseases; however, several clinical trial studies should be done to confirm its protective effects on humans.

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          Most cited references67

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          Platelet activation and atherothrombosis.

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            Atherosclerosis: Basic Mechanisms

            Circulation, 91(9), 2488-2496
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              Platelet adhesion signalling and the regulation of thrombus formation.

              Platelets perform a central role in haemostasis and thrombosis. They adhere to subendothelial collagens exposed at sites of blood vessel injury via the glycoprotein (GP) Ib-V-IX receptor complex, GPVI and integrin alpha(2)beta(1). These receptors perform distinct functions in the regulation of cell signalling involving non-receptor tyrosine kinases (e.g. Src, Fyn, Lyn, Syk and Btk), adaptor proteins, phospholipase C and lipid kinases such as phosphoinositide 3-kinase. They are also coupled to an increase in cytosolic calcium levels and protein kinase C activation, leading to the secretion of paracrine/autocrine platelet factors and an increase in integrin receptor affinities. Through the binding of plasma fibrinogen and von Willebrand Factor to integrin alpha(IIb)beta(3), a platelet thrombus is formed. Although increasing evidence indicates that each of the adhesion receptors GPIb-V-IX and GPVI and integrins alpha(2)beta(1) and alpha(IIb)beta(3) contribute to the signalling that regulates this process, the individual roles of each are only beginning to be dissected. By contrast, adhesion receptor signalling through platelet endothelial cell adhesion molecule 1 (PECAM-1) is implicated in the inhibition of platelet function and thrombus formation in the healthy circulation. Recent studies indicate that understanding of platelet adhesion signalling mechanisms might enable the development of new strategies to treat and prevent thrombosis.
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                Author and article information

                Journal
                Cardiovasc Hematol Agents Med Chem
                Cardiovasc Hematol Agents Med Chem
                CHAMC
                Cardiovascular & Hematological Agents in Medicinal Chemistry
                Bentham Science Publishers
                1871-5257
                1875-6182
                May 2019
                May 2019
                : 17
                : 1
                : 17-27
                Affiliations
                Cardiovascular Diseases Research Center, Birjand University of Medical Sciences , Birjand, , Iran;

                Noncommunicable Diseases Research Center, University of Medical Sciences , Neyshabur, , Iran;

                Department of Animal Science, Gorgan University of Agricultural Sciences and Natural Resources , Gorgan, , Iran
                Author notes
                [* ]Address correspondence to this author at the Noncommunicable Diseases Research Center, University of Medical Sciences, Neyshabur, Iran; Tel: +989151200945; E-mail: samarghandians1@ 123456nums.ac.ir
                Article
                CHAMC-17-17
                10.2174/1871525717666190114145137
                6865076
                30648526
                beffa940-50b3-46e0-83f8-80a1ae0d92dd
                © 2019 Bentham Science Publishers

                This is an open access article licensed under the terms of the Creative Commons Attribution-Non-Commercial 4.0 International Public License (CC BY-NC 4.0) ( https://creativecommons.org/licenses/by-nc/4.0/legalcode), which permits unrestricted, non-commercial use, distribution and reproduction in any medium, provided the work is properly cited.

                History
                : 06 November 2018
                : 25 December 2018
                : 02 January 2019
                Categories
                Article

                Cardiovascular Medicine
                antioxidant,apoptosis,cardiovascular disease,chrysin,inflammation,oxidative stress

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