{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,2,21]],"date-time":"2025-02-21T20:28:25Z","timestamp":1740169705730,"version":"3.37.3"},"reference-count":30,"publisher":"Wiley","license":[{"start":{"date-parts":[[2013,1,1]],"date-time":"2013-01-01T00:00:00Z","timestamp":1356998400000},"content-version":"unspecified","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/3.0\/"}],"funder":[{"DOI":"10.13039\/501100004826","name":"Beijing Natural Science Foundation","doi-asserted-by":"crossref","award":["7112012","2012XXGB01","CIT&TCD201304190"],"award-info":[{"award-number":["7112012","2012XXGB01","CIT&TCD201304190"]}],"id":[{"id":"10.13039\/501100004826","id-type":"DOI","asserted-by":"crossref"}]},{"name":"Scientific Research Foundation of Key Laboratory of Remodeling-Related Cardiovascular Diseases","award":["7112012","2012XXGB01","CIT&TCD201304190"],"award-info":[{"award-number":["7112012","2012XXGB01","CIT&TCD201304190"]}]},{"name":"Beijing Municipal Institutions","award":["7112012","2012XXGB01","CIT&TCD201304190"],"award-info":[{"award-number":["7112012","2012XXGB01","CIT&TCD201304190"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["BioMed Research International"],"published-print":{"date-parts":[[2013]]},"abstract":"<jats:p>Hyperhomocysteinemia is an independent risk factor for cardiovascular diseases. The enhanced nitrative stress plays an important role in homocysteine-induced endothelial dysfunction. Previous studies have showed that phytoestrogen<jats:italic>\u03b1<\/jats:italic>-zearalanol alleviated endothelial injury in ovariectomized hyperhomocysteinemic rats; however, the underlying mechanism remains to be clarified. This study was to investigate the effects of<jats:italic>\u03b1<\/jats:italic>-zearalanol on homocysteine-induced endothelial apoptosis<jats:italic>in vitro<\/jats:italic>and explore the possible role of nitrative stress in these effects. Results showed that homocysteine (500\u2009<jats:italic>\u03bc<\/jats:italic>mol\/L, 24\u2009h) induced the apoptosis of human umbilical vein endothelial cells (HUVECs) obviously, and this effect was significantly attenuated by pretreatment with<jats:italic>\u03b1<\/jats:italic>-zearalanol (10<jats:sup>\u22128<\/jats:sup>~10<jats:sup>\u22126<\/jats:sup>\u2009mol\/L). Moreover,<jats:italic>\u03b1<\/jats:italic>-zearalanol downregulated proapoptotic protein Bax, upregulated antiapoptotic proteins Bcl-2 and Bcl-XL, and decreased the expression and activity of caspase-9. These findings demonstrated that<jats:italic>\u03b1<\/jats:italic>-zearalanol could effectively alleviate homocysteine-induced endothelial apoptosis, and this antiapoptosis effect might be related to the inhibition of the intrinsic pathway. Western blot indicated an enhanced 3-nitrotyrosine expression in HUVECs when challenged with homocysteine, which was attenuated by pretreatment with<jats:italic>\u03b1<\/jats:italic>-zearalanol. This result implied that inhibition of nitrative stress might play a role in the protective effect of<jats:italic>\u03b1<\/jats:italic>-zearalanol on endothelial cells. Such discovery may shed a novel light on the antiatherogenic activities of<jats:italic>\u03b1<\/jats:italic>-zearalanol in hyperhomocysteinemia.<\/jats:p>","DOI":"10.1155\/2013\/813450","type":"journal-article","created":{"date-parts":[[2013,10,1]],"date-time":"2013-10-01T17:01:56Z","timestamp":1380646916000},"page":"1-12","source":"Crossref","is-referenced-by-count":8,"title":["Phytoestrogen<i>\u03b1<\/i>-Zearalanol Attenuates Homocysteine-Induced Apoptosis in Human Umbilical Vein Endothelial Cells"],"prefix":"10.1155","volume":"2013","author":[{"given":"Teng","family":"Liu","sequence":"first","affiliation":[{"name":"Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Capital Medical University, You An Men Wai, Fengtai District, Beijing 100069, China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Dan-dan","family":"Hou","sequence":"additional","affiliation":[{"name":"Department of Physiology and Pathophysiology, School of Basic Medical 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