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      Astragalus polysaccharide ameliorates H 2O 2-induced human umbilical vein endothelial cell injury

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          Abstract

          Endothelial dysfunction caused by reactive oxygen species (ROS) has been implicated in numerous cardiovascular diseases. Astragalus polysaccharide (APS), an important bioactive component extracted from the Chinese herb Astragalus membranaceus, has been widely used for the treatment of cardiovascular disease. The present study aimed to investigate the effects of APS on hydrogen peroxide (H 2O 2)-induced human umbilical vein endothelial cell (HUVEC) injury. Following treatment with 400 µM H 2O 2 for 24 h, cell viability was decreased and apoptosis was increased. However, pretreatment with APS for 1 h significantly attenuated H 2O 2-induced injury in HUVECs. In addition, APS decreased intracellular ROS levels, increased the protein expression of endothelial nitric oxide synthase and copper-zinc superoxide dismutase, elevated intracellular cyclic guanosine monophosphate (an activity marker for nitric oxide) levels and restored the mitochondrial membrane potential, compared with cells treated with H 2O 2 only. In conclusion, the results of the present study suggested that APS may protect HUVECs from injury induced by H 2O 2 via increasing the cell antioxidant capacity and nitric oxide (NO) bioavailability, which may contribute to the improvement of the imbalance between ROS and NO levels.

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          Role of oxidative stress in atherosclerosis

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            Reactive oxygen species in vascular biology: implications in hypertension.

            Reactive oxygen species (ROS), including superoxide (*O2-), hydrogen peroxide (H2O2), and hydroxyl anion (OH-), and reactive nitrogen species, such as nitric oxide (NO) and peroxynitrite (ONOO-), are biologically important O2 derivatives that are increasingly recognized to be important in vascular biology through their oxidation/reduction (redox) potential. All vascular cell types (endothelial cells, vascular smooth muscle cells, and adventitial fibroblasts) produce ROS, primarily via cell membrane-associated NAD(P)H oxidase. Reactive oxygen species regulate vascular function by modulating cell growth, apoptosis/anoikis, migration, inflammation, secretion, and extracellular matrix protein production. An imbalance in redox state where pro-oxidants overwhelm anti-oxidant capacity results in oxidative stress. Oxidative stress and associated oxidative damage are mediators of vascular injury and inflammation in many cardiovascular diseases, including hypertension, hyperlipidemia, and diabetes. Increased generation of ROS has been demonstrated in experimental and human hypertension. Anti-oxidants and agents that interrupt NAD(P)H oxidase-driven *O2- production regress vascular remodeling, improve endothelial function, reduce inflammation, and decrease blood pressure in hypertensive models. This experimental evidence has evoked considerable interest because of the possibilities that therapies targeted against reactive oxygen intermediates, by decreasing generation of ROS and/or by increasing availability of antioxidants, may be useful in minimizing vascular injury and hypertensive end organ damage. The present chapter focuses on the importance of ROS in vascular biology and discusses the role of oxidative stress in vascular damage in hypertension.
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              Endothelial function: a barometer for cardiovascular risk?

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                Author and article information

                Journal
                Mol Med Rep
                Mol Med Rep
                Molecular Medicine Reports
                D.A. Spandidos
                1791-2997
                1791-3004
                June 2017
                26 April 2017
                26 April 2017
                : 15
                : 6
                : 4027-4034
                Affiliations
                [1 ]Key Laboratory of Cardiovascular and Cerebrovascular Drug Research of Liaoning Province, Drug Research Institute, Jinzhou Medical University, Jinzhou, Liaoning 121001, P.R. China
                [2 ]Department of Pharmacology, Key Laboratory of Cardiovascular and Cerebrovascular Drug Research of Liaoning Drug Research Institute, Jinzhou Medical University, Jinzhou, Liaoning 121001, P.R. China
                Author notes
                Correspondence to: Professor Hongxin Wang, Department of Pharmacology, Key Laboratory of Cardiovascular and Cerebrovascular Drug Research of Liaoning Drug Research Institute, Jinzhou Medical University, 40 Songpo Road, Jinzhou, Liaoning 121001, P.R. China, E-mail: jyhxwang@ 123456163.com
                Article
                mmr-15-06-4027
                10.3892/mmr.2017.6515
                5436204
                28487940
                729d2d05-affd-4dd1-8eaf-570defc4996d
                Copyright: © Han et al.

                This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

                History
                : 02 February 2016
                : 20 February 2017
                Categories
                Articles

                astragalus polysaccharide,human umbilical vein endothelial cells,oxidative stress,nitric oxide,apoptosis

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