title: Salidroside Suppresses HUVECs Cell Injury Induced by Oxidative Stress through Activating the Nrf2 Signaling Pathway.
abstract: Oxidative stress plays an important role in the pathogenesis of cardiovascular diseases. Salidroside (SAL), one of the main effective constituents of Rhodiola rosea, has been reported to suppress oxidative stress-induced cardiomyocyte injury and necrosis by promoting transcription of nuclear factor E2-related factor 2 (Nrf2)-regulated genes such as heme oxygenase-1 (HO-1) and NAD(P)H dehydrogenase (quinone1) (NQO1). However, it has not been indicated whether SAL might ameliorate endothelial injury induced by oxidative stress. Here, our study demonstrated that SAL might suppress HUVEC cell injury induced by oxidative stress through activating the Nrf2 signaling pathway. The results of our study indicated that SAL decreased the levels of intercellular reactive oxygen species (ROS) and malondialdehyde (MDA), and improved the activities of superoxide dismutase (SOD) and catalase (CAT), resulting in protective effects against oxidative stress-induced cell damage in HUVECs. It suppressed oxidative stress damage by inducing Nrf2 nuclear translocation and activating the expression of Nrf2-regulated antioxidant enzyme genes such as HO-1 and NQO1 in HUVECs. Knockdown of Nrf2 with siRNA abolished the cytoprotective effects against oxidative stress, decreased the expression of Nrf2, HO-1, and NQO1, and inhibited the nucleus translocation of Nrf2 in HUVECs. This study is the first to demonstrate that SAL suppresses HUVECs cell injury induced by oxidative stress through activating the Nrf2 signaling pathway.
authors: First College of Clinical Medicine, Nanjing University of Traditional Chinese Medicine, Nanjing 210023, China. zy_njtcm@126.com.
authors: Yao
authors: Y
authors: Zhu
authors: Nanjing Hospital of Traditional Chinese Medicine, Nanjing 210001, China. zhangyajie_jack@126.com.
authors: Ya-Jie
authors: YJ
authors: Zhang
authors: First College of Clinical Medicine, Nanjing University of Traditional Chinese Medicine, Nanjing 210023, China. cheeseweiweiliu@126.com.
authors: Wei-Wei
authors: WW
authors: Liu
authors: Nanjing Maternity and Child Health Care Hospital, Nanjing 210004, China. shiaiwu888@163.com.
authors: Ai-Wu
authors: AW
authors: Shi
authors: Nanjing Hospital of Traditional Chinese Medicine, Nanjing 210001, China. jsguning@163.com.
authors: Ning
authors: N
authors: Gu
mesh_terms: D002374:Catalase / Q000096:biosynthesis; D005960:Glucosides / Q000494:pharmacology*; D051547:Heme Oxygenase-1 / Q000096:biosynthesis; D061307:Human Umbilical Vein Endothelial Cells / Q000378:metabolism* / Q000473:pathology; D008315:Malondialdehyde / Q000378:metabolism; D016660:NAD(P)H Dehydrogenase (Quinone) / Q000096:biosynthesis; D051267:NF-E2-Related Factor 2 / Q000378:metabolism*; D018384:Oxidative Stress / Q000187:drug effects*; D010636:Phenols / Q000494:pharmacology*; D017382:Reactive Oxygen Species / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects*; D013482:Superoxide Dismutase / Q000096:biosynthesis
chemical_list: D005960:Glucosides; D051267:NF-E2-Related Factor 2; C495635:NFE2L2 protein, human; D010636:Phenols; D017382:Reactive Oxygen Species; D008315:Malondialdehyde; D002374:Catalase; C496541:HMOX1 protein, human; D051547:Heme Oxygenase-1; D013482:Superoxide Dismutase; D016660:NAD(P)H Dehydrogenase (Quinone); C447479:NQO1 protein, human; C009172:rhodioloside
keywords: NAD(P)H dehydrogenase (quinone1); heme oxygenase-1; human umbilical vein endothelial cells; nuclear factor E2-related factor 2; oxidative stress; salidroside