Astragalus polysaccharide ameliorates H2O2-induced human umbilical vein endothelial cell injury
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...
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Veröffentlicht in: | Molecular medicine reports 2017-06, Vol.15 (6), p.4027-4034 |
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description | 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 (H2O2)‑induced human umbilical vein endothelial cell (HUVEC) injury. Following treatment with 400 µM H2O2 for 24 h, cell viability was decreased and apoptosis was increased. However, pretreatment with APS for 1 h significantly attenuated H2O2‑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 H2O2 only. In conclusion, the results of the present study suggested that APS may protect HUVECs from injury induced by H2O2 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. |
doi_str_mv | 10.3892/mmr.2017.6515 |
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fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_5436204</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1899104491</sourcerecordid><originalsourceid>FETCH-LOGICAL-c415t-b9ddd0c21898ebce6eefc45a1fc68c7a0ae73a6687a9f38a23171238a563223f3</originalsourceid><addsrcrecordid>eNpdkTtrHDEURoVJiF8p3YaBNGlmo8fo1QSMSeyAwU1cC63mjleLRtpII8P-e2vxxiSpdJGOPu7HQeiK4BVTmn6d57yimMiV4ISfoDMiNekZxsO740y1lqfovJQtxoJTrj-gU6oGJfWAz5C5Lku2TzbU0u1S2Bfr3MZmP0JnZwg-ZbtA6e7oA-19HKuDsdvU2cauzmsfvLOhewYfO4hjWjbtR7twEELn47bm_SV6P9lQ4OPxvECPP77_urnr7x9uf95c3_duIHzp13ocR-woUVrB2oEAmNzALZmcUE5abEEyK4SSVk9MWcqIJLQNXDBK2cQu0LfX3F1dzzA6iK1WMLvsZ5v3Jllv_n2JfmOe0rPhAxMUDy3gyzEgp98VymJmXw5FbIRUi2mbaYKHQZOGfv4P3aaaY6tniBaUKyopb1T_SrmcSskwvS1DsDmoM02dOagzB3WN__R3gzf6jyv2Al0Nluk</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1962582725</pqid></control><display><type>article</type><title>Astragalus polysaccharide ameliorates H2O2-induced human umbilical vein endothelial cell injury</title><source>Spandidos Publications Journals</source><source>MEDLINE</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>Alma/SFX Local Collection</source><creator>Han, Ronghui ; Tang, Futian ; Lu, Meili ; Xu, Chonghua ; Hu, Jin ; Mei, Meng ; Wang, Hongxin</creator><creatorcontrib>Han, Ronghui ; Tang, Futian ; Lu, Meili ; Xu, Chonghua ; Hu, Jin ; Mei, Meng ; Wang, Hongxin</creatorcontrib><description>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 (H2O2)‑induced human umbilical vein endothelial cell (HUVEC) injury. Following treatment with 400 µM H2O2 for 24 h, cell viability was decreased and apoptosis was increased. However, pretreatment with APS for 1 h significantly attenuated H2O2‑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 H2O2 only. In conclusion, the results of the present study suggested that APS may protect HUVECs from injury induced by H2O2 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.</description><identifier>ISSN: 1791-2997</identifier><identifier>EISSN: 1791-3004</identifier><identifier>DOI: 10.3892/mmr.2017.6515</identifier><identifier>PMID: 28487940</identifier><language>eng</language><publisher>Greece: Spandidos Publications UK Ltd</publisher><subject>Angiogenesis ; Antioxidants ; Antioxidants - pharmacology ; Apoptosis ; Apoptosis - drug effects ; Astragalus ; Astragalus Plant - chemistry ; Bioavailability ; Biotechnology ; Cardiovascular diseases ; Cell cycle ; Cell injury ; Cell Survival - drug effects ; Cells, Cultured ; Chinese medicine ; Cyclic GMP ; Cyclic GMP - metabolism ; Endothelial cells ; Endothelium ; Guanosine ; Human Umbilical Vein Endothelial Cells - drug effects ; Human Umbilical Vein Endothelial Cells - metabolism ; Humans ; Hydrogen peroxide ; Hydrogen Peroxide - pharmacology ; Intracellular ; Membrane potential ; Membrane Potential, Mitochondrial - drug effects ; Mitochondria ; Nitric oxide ; Nitric Oxide - metabolism ; Nitric Oxide Synthase Type III - metabolism ; Nitric-oxide synthase ; Oxidative stress ; Oxidative Stress - drug effects ; Plant Extracts - pharmacology ; Polysaccharides - pharmacology ; Protein expression ; Proteins ; Reactive oxygen species ; Reactive Oxygen Species - metabolism ; Rodents ; Studies ; Superoxide dismutase ; Superoxide Dismutase - metabolism ; Umbilical vein</subject><ispartof>Molecular medicine reports, 2017-06, Vol.15 (6), p.4027-4034</ispartof><rights>Copyright Spandidos Publications UK Ltd. 2017</rights><rights>Copyright: © Han et al. 2017</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c415t-b9ddd0c21898ebce6eefc45a1fc68c7a0ae73a6687a9f38a23171238a563223f3</citedby><cites>FETCH-LOGICAL-c415t-b9ddd0c21898ebce6eefc45a1fc68c7a0ae73a6687a9f38a23171238a563223f3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28487940$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Han, Ronghui</creatorcontrib><creatorcontrib>Tang, Futian</creatorcontrib><creatorcontrib>Lu, Meili</creatorcontrib><creatorcontrib>Xu, Chonghua</creatorcontrib><creatorcontrib>Hu, Jin</creatorcontrib><creatorcontrib>Mei, Meng</creatorcontrib><creatorcontrib>Wang, Hongxin</creatorcontrib><title>Astragalus polysaccharide ameliorates H2O2-induced human umbilical vein endothelial cell injury</title><title>Molecular medicine reports</title><addtitle>Mol Med Rep</addtitle><description>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 (H2O2)‑induced human umbilical vein endothelial cell (HUVEC) injury. Following treatment with 400 µM H2O2 for 24 h, cell viability was decreased and apoptosis was increased. However, pretreatment with APS for 1 h significantly attenuated H2O2‑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 H2O2 only. In conclusion, the results of the present study suggested that APS may protect HUVECs from injury induced by H2O2 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.</description><subject>Angiogenesis</subject><subject>Antioxidants</subject><subject>Antioxidants - pharmacology</subject><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Astragalus</subject><subject>Astragalus Plant - chemistry</subject><subject>Bioavailability</subject><subject>Biotechnology</subject><subject>Cardiovascular diseases</subject><subject>Cell cycle</subject><subject>Cell injury</subject><subject>Cell Survival - drug effects</subject><subject>Cells, Cultured</subject><subject>Chinese medicine</subject><subject>Cyclic GMP</subject><subject>Cyclic GMP - metabolism</subject><subject>Endothelial cells</subject><subject>Endothelium</subject><subject>Guanosine</subject><subject>Human Umbilical Vein Endothelial Cells - drug effects</subject><subject>Human Umbilical Vein Endothelial Cells - metabolism</subject><subject>Humans</subject><subject>Hydrogen peroxide</subject><subject>Hydrogen Peroxide - pharmacology</subject><subject>Intracellular</subject><subject>Membrane potential</subject><subject>Membrane Potential, Mitochondrial - drug effects</subject><subject>Mitochondria</subject><subject>Nitric oxide</subject><subject>Nitric Oxide - metabolism</subject><subject>Nitric Oxide Synthase Type III - metabolism</subject><subject>Nitric-oxide synthase</subject><subject>Oxidative stress</subject><subject>Oxidative Stress - drug effects</subject><subject>Plant Extracts - pharmacology</subject><subject>Polysaccharides - pharmacology</subject><subject>Protein expression</subject><subject>Proteins</subject><subject>Reactive oxygen species</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Rodents</subject><subject>Studies</subject><subject>Superoxide dismutase</subject><subject>Superoxide Dismutase - metabolism</subject><subject>Umbilical vein</subject><issn>1791-2997</issn><issn>1791-3004</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNpdkTtrHDEURoVJiF8p3YaBNGlmo8fo1QSMSeyAwU1cC63mjleLRtpII8P-e2vxxiSpdJGOPu7HQeiK4BVTmn6d57yimMiV4ISfoDMiNekZxsO740y1lqfovJQtxoJTrj-gU6oGJfWAz5C5Lku2TzbU0u1S2Bfr3MZmP0JnZwg-ZbtA6e7oA-19HKuDsdvU2cauzmsfvLOhewYfO4hjWjbtR7twEELn47bm_SV6P9lQ4OPxvECPP77_urnr7x9uf95c3_duIHzp13ocR-woUVrB2oEAmNzALZmcUE5abEEyK4SSVk9MWcqIJLQNXDBK2cQu0LfX3F1dzzA6iK1WMLvsZ5v3Jllv_n2JfmOe0rPhAxMUDy3gyzEgp98VymJmXw5FbIRUi2mbaYKHQZOGfv4P3aaaY6tniBaUKyopb1T_SrmcSskwvS1DsDmoM02dOagzB3WN__R3gzf6jyv2Al0Nluk</recordid><startdate>20170601</startdate><enddate>20170601</enddate><creator>Han, Ronghui</creator><creator>Tang, Futian</creator><creator>Lu, Meili</creator><creator>Xu, Chonghua</creator><creator>Hu, Jin</creator><creator>Mei, Meng</creator><creator>Wang, Hongxin</creator><general>Spandidos Publications UK Ltd</general><general>D.A. 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pharmacology</topic><topic>Apoptosis</topic><topic>Apoptosis - drug effects</topic><topic>Astragalus</topic><topic>Astragalus Plant - chemistry</topic><topic>Bioavailability</topic><topic>Biotechnology</topic><topic>Cardiovascular diseases</topic><topic>Cell cycle</topic><topic>Cell injury</topic><topic>Cell Survival - drug effects</topic><topic>Cells, Cultured</topic><topic>Chinese medicine</topic><topic>Cyclic GMP</topic><topic>Cyclic GMP - metabolism</topic><topic>Endothelial cells</topic><topic>Endothelium</topic><topic>Guanosine</topic><topic>Human Umbilical Vein Endothelial Cells - drug effects</topic><topic>Human Umbilical Vein Endothelial Cells - metabolism</topic><topic>Humans</topic><topic>Hydrogen peroxide</topic><topic>Hydrogen Peroxide - pharmacology</topic><topic>Intracellular</topic><topic>Membrane potential</topic><topic>Membrane Potential, Mitochondrial - drug effects</topic><topic>Mitochondria</topic><topic>Nitric oxide</topic><topic>Nitric Oxide - metabolism</topic><topic>Nitric Oxide Synthase Type III - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Molecular medicine reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Han, Ronghui</au><au>Tang, Futian</au><au>Lu, Meili</au><au>Xu, Chonghua</au><au>Hu, Jin</au><au>Mei, Meng</au><au>Wang, Hongxin</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Astragalus polysaccharide ameliorates H2O2-induced human umbilical vein endothelial cell injury</atitle><jtitle>Molecular medicine reports</jtitle><addtitle>Mol Med Rep</addtitle><date>2017-06-01</date><risdate>2017</risdate><volume>15</volume><issue>6</issue><spage>4027</spage><epage>4034</epage><pages>4027-4034</pages><issn>1791-2997</issn><eissn>1791-3004</eissn><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 (H2O2)‑induced human umbilical vein endothelial cell (HUVEC) injury. Following treatment with 400 µM H2O2 for 24 h, cell viability was decreased and apoptosis was increased. However, pretreatment with APS for 1 h significantly attenuated H2O2‑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 H2O2 only. In conclusion, the results of the present study suggested that APS may protect HUVECs from injury induced by H2O2 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.</abstract><cop>Greece</cop><pub>Spandidos Publications UK Ltd</pub><pmid>28487940</pmid><doi>10.3892/mmr.2017.6515</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Angiogenesis Antioxidants Antioxidants - pharmacology Apoptosis Apoptosis - drug effects Astragalus Astragalus Plant - chemistry Bioavailability Biotechnology Cardiovascular diseases Cell cycle Cell injury Cell Survival - drug effects Cells, Cultured Chinese medicine Cyclic GMP Cyclic GMP - metabolism Endothelial cells Endothelium Guanosine Human Umbilical Vein Endothelial Cells - drug effects Human Umbilical Vein Endothelial Cells - metabolism Humans Hydrogen peroxide Hydrogen Peroxide - pharmacology Intracellular Membrane potential Membrane Potential, Mitochondrial - drug effects Mitochondria Nitric oxide Nitric Oxide - metabolism Nitric Oxide Synthase Type III - metabolism Nitric-oxide synthase Oxidative stress Oxidative Stress - drug effects Plant Extracts - pharmacology Polysaccharides - pharmacology Protein expression Proteins Reactive oxygen species Reactive Oxygen Species - metabolism Rodents Studies Superoxide dismutase Superoxide Dismutase - metabolism Umbilical vein |
title | Astragalus polysaccharide ameliorates H2O2-induced human umbilical vein endothelial cell injury |
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