{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,30]],"date-time":"2026-10-30T04:07:56Z","timestamp":1793333276125,"version":"4.5.0"},"reference-count":25,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2016,12,13]],"date-time":"2016-12-13T00:00:00Z","timestamp":1481587200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["81300220"],"award-info":[{"award-number":["81300220"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Cardiovascular Therapeutics"],"published-print":{"date-parts":[[2017,2]]},"abstract":"<jats:title>Summary<\/jats:title><jats:sec><jats:title>Introduction<\/jats:title><jats:p>Previous studies showed that homocysteine (Hcy) could injure vascular endothelial cells via several mechanisms, including its promotion of oxidative stress pathway and endoplasmic reticulum stress (<jats:styled-content style=\"fixed-case\">ER<\/jats:styled-content> stress) pathway. Salidroside (<jats:styled-content style=\"fixed-case\">SAL<\/jats:styled-content>) is an active component of Rhodiola rosea with documented antioxidative properties. Emerging evidence conformed that <jats:styled-content style=\"fixed-case\">SAL<\/jats:styled-content> attenuated Hcy\u2010induced endothelial dysfunction by reducing oxidative stress. However, its role in <jats:styled-content style=\"fixed-case\">ER<\/jats:styled-content> stress pathway remains unclarified.<\/jats:p><\/jats:sec><jats:sec><jats:title>Aims<\/jats:title><jats:p>The purpose of this study was to explore the mechanism of the protective effect of <jats:styled-content style=\"fixed-case\">SAL<\/jats:styled-content> on Hcy\u2010induced endothelial dysfunction.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Pretreatment of the human umbilical vein endothelial cells (<jats:styled-content style=\"fixed-case\">HUVEC<\/jats:styled-content>s) with <jats:styled-content style=\"fixed-case\">SAL<\/jats:styled-content> significantly reduced the cell damage effects brought by Hcy in a dose\u2010dependent manner. Functional studies on the <jats:styled-content style=\"fixed-case\">HUVEC<\/jats:styled-content>s found that <jats:styled-content style=\"fixed-case\">SAL<\/jats:styled-content> rescued the endoplasmic reticulum stress induced by Hcy. The underlying mechanisms involve the inhibition of Hcy\u2010induced activation of binding protein (Bip) and C\/<jats:styled-content style=\"fixed-case\">EBP<\/jats:styled-content> homologous protein (<jats:styled-content style=\"fixed-case\">CHOP<\/jats:styled-content>), as well as the phosphorylation of protein kinase <jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content>\u2010like <jats:styled-content style=\"fixed-case\">ER<\/jats:styled-content> kinase (<jats:styled-content style=\"fixed-case\">PERK<\/jats:styled-content>) or inositol\u2010requiring enzyme 1 alpha (<jats:styled-content style=\"fixed-case\">IRE<\/jats:styled-content>1\u03b1).<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>Taken together, these findings implicate that <jats:styled-content style=\"fixed-case\">SAL<\/jats:styled-content> could regulate <jats:styled-content style=\"fixed-case\">ER<\/jats:styled-content> stress pathway on the viability of endotheliocyte induced by Hcy in vitro. Our findings provide the first evidence that <jats:styled-content style=\"fixed-case\">SAL<\/jats:styled-content> plays an important role in endotheliocyte protection via suppressing <jats:styled-content style=\"fixed-case\">ER<\/jats:styled-content> stress pathway in <jats:styled-content style=\"fixed-case\">HUVEC<\/jats:styled-content> cells and that it may be a promising therapeutic target for atherosclerosis and cardiovascular disease.<\/jats:p><\/jats:sec>","DOI":"10.1111\/1755-5922.12234","type":"journal-article","created":{"date-parts":[[2016,11,3]],"date-time":"2016-11-03T13:27:36Z","timestamp":1478179656000},"page":"33-39","source":"Crossref","is-referenced-by-count":31,"title":["Salidroside protects against homocysteine\u2010induced injury in human umbilical vein endothelial cells via the regulation of endoplasmic reticulum stress"],"prefix":"10.1111","volume":"35","author":[{"given":"Lin","family":"Zhu","sequence":"first","affiliation":[{"name":"Department of Cardiology 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