Protective Effects of Salidroside on Endothelial Cell Apoptosis Induced by Cobalt Chloride
Salidroside is a major constituent of Rhodiola rosea L. that elicits beneficial effects for ischemic cardiovascular diseases. The aim of this study was to investigate the protective effects of salidroside on endothelial cells apoptosis induced by the hypoxia mimicking agent, cobalt chloride. After c...
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| Veröffentlicht in: | Biological & Pharmaceutical Bulletin 2009/08/01, Vol.32(8), pp.1359-1363 |
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| creator | Tan, Chu-Bing Gao, Mei Xu, Wei-Ren Yang, Xiu-Ying Zhu, Xiao-Ming Du, Guan-Hua |
| description | Salidroside is a major constituent of Rhodiola rosea L. that elicits beneficial effects for ischemic cardiovascular diseases. The aim of this study was to investigate the protective effects of salidroside on endothelial cells apoptosis induced by the hypoxia mimicking agent, cobalt chloride. After challenge with cobalt chloride for 24 h, loss of cell viability and excessive apoptotic cell death were observed in EA.hy926 endothelial cells, and the level of intracellular reactive oxygen species (ROS) increased concentration-dependently. However, the endothelial cell apoptosis and excessive ROS generation were attenuated markedly by salidroside pretreatment. In addition, salidroside inhibited activation of caspase-3 and cleavage of poly(ADP-ribose) polymerase (PARP) induced by cobalt chloride, decreased expression of Bax and rescued the balance of pro- and anti-apoptotic proteins. These findings suggest that salidroside protects endothelial cells from cobalt chloride-induced apoptosis as an antioxidant and by regulating Bcl-2 family. Salidroside may represent a novel therapeutic agent for the treatment and prevention of hypoxia and oxidative stress-related diseases. |
| doi_str_mv | 10.1248/bpb.32.1359 |
| format | Article |
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The aim of this study was to investigate the protective effects of salidroside on endothelial cells apoptosis induced by the hypoxia mimicking agent, cobalt chloride. After challenge with cobalt chloride for 24 h, loss of cell viability and excessive apoptotic cell death were observed in EA.hy926 endothelial cells, and the level of intracellular reactive oxygen species (ROS) increased concentration-dependently. However, the endothelial cell apoptosis and excessive ROS generation were attenuated markedly by salidroside pretreatment. In addition, salidroside inhibited activation of caspase-3 and cleavage of poly(ADP-ribose) polymerase (PARP) induced by cobalt chloride, decreased expression of Bax and rescued the balance of pro- and anti-apoptotic proteins. These findings suggest that salidroside protects endothelial cells from cobalt chloride-induced apoptosis as an antioxidant and by regulating Bcl-2 family. Salidroside may represent a novel therapeutic agent for the treatment and prevention of hypoxia and oxidative stress-related diseases.</description><identifier>ISSN: 0918-6158</identifier><identifier>EISSN: 1347-5215</identifier><identifier>DOI: 10.1248/bpb.32.1359</identifier><identifier>PMID: 19652374</identifier><language>eng</language><publisher>Japan: The Pharmaceutical Society of Japan</publisher><subject>Antioxidants - chemistry ; Antioxidants - pharmacology ; apoptosis ; Apoptosis - drug effects ; bcl-2-Associated X Protein - biosynthesis ; Blotting, Western ; Caspase 3 - biosynthesis ; Caspase 3 - metabolism ; Cell Culture Techniques ; Cell Hypoxia - drug effects ; Cell Line ; Cell Survival - drug effects ; Cobalt - toxicity ; cobalt chloride ; Dose-Response Relationship, Drug ; endothelial cell ; Endothelial Cells - drug effects ; Endothelial Cells - metabolism ; Endothelial Cells - pathology ; Endothelium, Vascular - drug effects ; Endothelium, Vascular - metabolism ; Endothelium, Vascular - pathology ; Flow Cytometry ; Glucosides - chemistry ; Glucosides - pharmacology ; Humans ; Hypoxia-Inducible Factor 1, alpha Subunit - biosynthesis ; Molecular Structure ; Phenols - chemistry ; Phenols - pharmacology ; Proto-Oncogene Proteins c-bcl-2 - biosynthesis ; Reactive Oxygen Species - metabolism ; salidroside</subject><ispartof>Biological and Pharmaceutical Bulletin, 2009/08/01, Vol.32(8), pp.1359-1363</ispartof><rights>2009 The Pharmaceutical Society of Japan</rights><rights>Copyright Japan Science and Technology Agency 2009</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c690t-c63e3a926818f4161acc640a900773187695c993417cfb3c46459625d2d6d0223</citedby><cites>FETCH-LOGICAL-c690t-c63e3a926818f4161acc640a900773187695c993417cfb3c46459625d2d6d0223</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,1883,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19652374$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Tan, Chu-Bing</creatorcontrib><creatorcontrib>Gao, Mei</creatorcontrib><creatorcontrib>Xu, Wei-Ren</creatorcontrib><creatorcontrib>Yang, Xiu-Ying</creatorcontrib><creatorcontrib>Zhu, Xiao-Ming</creatorcontrib><creatorcontrib>Du, Guan-Hua</creatorcontrib><creatorcontrib>Chinese Academy of Medical Sciences and Peking Union Medical College</creatorcontrib><creatorcontrib>aInstitute of Materia Medica</creatorcontrib><creatorcontrib>bTianjin key Lab of Molecular Design and Drug Discovery</creatorcontrib><creatorcontrib>Tianjin Institute of Pharmaceutical Research</creatorcontrib><title>Protective Effects of Salidroside on Endothelial Cell Apoptosis Induced by Cobalt Chloride</title><title>Biological & Pharmaceutical Bulletin</title><addtitle>Biol Pharm Bull</addtitle><description>Salidroside is a major constituent of Rhodiola rosea L. that elicits beneficial effects for ischemic cardiovascular diseases. The aim of this study was to investigate the protective effects of salidroside on endothelial cells apoptosis induced by the hypoxia mimicking agent, cobalt chloride. After challenge with cobalt chloride for 24 h, loss of cell viability and excessive apoptotic cell death were observed in EA.hy926 endothelial cells, and the level of intracellular reactive oxygen species (ROS) increased concentration-dependently. However, the endothelial cell apoptosis and excessive ROS generation were attenuated markedly by salidroside pretreatment. In addition, salidroside inhibited activation of caspase-3 and cleavage of poly(ADP-ribose) polymerase (PARP) induced by cobalt chloride, decreased expression of Bax and rescued the balance of pro- and anti-apoptotic proteins. These findings suggest that salidroside protects endothelial cells from cobalt chloride-induced apoptosis as an antioxidant and by regulating Bcl-2 family. Salidroside may represent a novel therapeutic agent for the treatment and prevention of hypoxia and oxidative stress-related diseases.</description><subject>Antioxidants - chemistry</subject><subject>Antioxidants - pharmacology</subject><subject>apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>bcl-2-Associated X Protein - biosynthesis</subject><subject>Blotting, Western</subject><subject>Caspase 3 - biosynthesis</subject><subject>Caspase 3 - metabolism</subject><subject>Cell Culture Techniques</subject><subject>Cell Hypoxia - drug effects</subject><subject>Cell Line</subject><subject>Cell Survival - drug effects</subject><subject>Cobalt - toxicity</subject><subject>cobalt chloride</subject><subject>Dose-Response Relationship, Drug</subject><subject>endothelial cell</subject><subject>Endothelial Cells - drug effects</subject><subject>Endothelial Cells - metabolism</subject><subject>Endothelial Cells - pathology</subject><subject>Endothelium, Vascular - drug effects</subject><subject>Endothelium, Vascular - metabolism</subject><subject>Endothelium, Vascular - pathology</subject><subject>Flow Cytometry</subject><subject>Glucosides - chemistry</subject><subject>Glucosides - pharmacology</subject><subject>Humans</subject><subject>Hypoxia-Inducible Factor 1, alpha Subunit - biosynthesis</subject><subject>Molecular Structure</subject><subject>Phenols - chemistry</subject><subject>Phenols - pharmacology</subject><subject>Proto-Oncogene Proteins c-bcl-2 - biosynthesis</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>salidroside</subject><issn>0918-6158</issn><issn>1347-5215</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkM1rFEEQxRtRzBo9eZcGDznIbvr742YYNhoIGFAvXpqenh63l97psXsmkP8-vc7GgJeqgvrVq8cD4D1GG0yYumzHdkPJBlOuX4AVpkyuOcH8JVghjdVaYK7OwJtS9gghiQh9Dc6wFpxQyVbg111Ok3dTuPdw2_d1KjD18LuNocuphM7DNMDt0KVp52OwETY-Rng1pnGq6wJvhm52voPtA2xSa-MEm11MuR6-Ba96G4t_d-rn4Of19kfzdX377ctNc3W7dkKjqVbqqdVEKKx6hgW2zgmGrK5uJcVKCs2d1pRh6fqWOiYY14LwjnSiQ4TQc3Cx6I45_Zl9mcwhFFdd2sGnuRhJKZecc1zJj_-R-zTnoZozmDFdA8FYVurTQrkaQMm-N2MOB5sfDEbmmLipiRtKzDHxSn84ac7twXfP7CniClwvQN0GZ2MaYhj882dXZBtSTIYgpA1ClCBljuNRvhZBlUQcqyr0eRHal8n-9v8-2TwFF_2TK7WUv9dPK7ez2fiBPgLVI6bU</recordid><startdate>20090801</startdate><enddate>20090801</enddate><creator>Tan, Chu-Bing</creator><creator>Gao, Mei</creator><creator>Xu, Wei-Ren</creator><creator>Yang, Xiu-Ying</creator><creator>Zhu, Xiao-Ming</creator><creator>Du, Guan-Hua</creator><general>The Pharmaceutical Society of Japan</general><general>Pharmaceutical Society of Japan</general><general>Japan Science and Technology Agency</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QP</scope><scope>7QR</scope><scope>7TK</scope><scope>7U9</scope><scope>8FD</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><scope>7X8</scope></search><sort><creationdate>20090801</creationdate><title>Protective Effects of Salidroside on Endothelial Cell Apoptosis Induced by Cobalt Chloride</title><author>Tan, Chu-Bing ; 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The aim of this study was to investigate the protective effects of salidroside on endothelial cells apoptosis induced by the hypoxia mimicking agent, cobalt chloride. After challenge with cobalt chloride for 24 h, loss of cell viability and excessive apoptotic cell death were observed in EA.hy926 endothelial cells, and the level of intracellular reactive oxygen species (ROS) increased concentration-dependently. However, the endothelial cell apoptosis and excessive ROS generation were attenuated markedly by salidroside pretreatment. In addition, salidroside inhibited activation of caspase-3 and cleavage of poly(ADP-ribose) polymerase (PARP) induced by cobalt chloride, decreased expression of Bax and rescued the balance of pro- and anti-apoptotic proteins. These findings suggest that salidroside protects endothelial cells from cobalt chloride-induced apoptosis as an antioxidant and by regulating Bcl-2 family. Salidroside may represent a novel therapeutic agent for the treatment and prevention of hypoxia and oxidative stress-related diseases.</abstract><cop>Japan</cop><pub>The Pharmaceutical Society of Japan</pub><pmid>19652374</pmid><doi>10.1248/bpb.32.1359</doi><tpages>5</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Antioxidants - chemistry Antioxidants - pharmacology apoptosis Apoptosis - drug effects bcl-2-Associated X Protein - biosynthesis Blotting, Western Caspase 3 - biosynthesis Caspase 3 - metabolism Cell Culture Techniques Cell Hypoxia - drug effects Cell Line Cell Survival - drug effects Cobalt - toxicity cobalt chloride Dose-Response Relationship, Drug endothelial cell Endothelial Cells - drug effects Endothelial Cells - metabolism Endothelial Cells - pathology Endothelium, Vascular - drug effects Endothelium, Vascular - metabolism Endothelium, Vascular - pathology Flow Cytometry Glucosides - chemistry Glucosides - pharmacology Humans Hypoxia-Inducible Factor 1, alpha Subunit - biosynthesis Molecular Structure Phenols - chemistry Phenols - pharmacology Proto-Oncogene Proteins c-bcl-2 - biosynthesis Reactive Oxygen Species - metabolism salidroside |
| title | Protective Effects of Salidroside on Endothelial Cell Apoptosis Induced by Cobalt Chloride |
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