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Molecules 2016, 21(8), 1033; doi:10.3390/molecules21081033

Salidroside Suppresses HUVECs Cell Injury Induced by Oxidative Stress through Activating the Nrf2 Signaling Pathway

1,†
,
2,†
,
1
,
3,* and 2,*
1
First College of Clinical Medicine, Nanjing University of Traditional Chinese Medicine, Nanjing 210023, China
2
Nanjing Hospital of Traditional Chinese Medicine, Nanjing 210001, China
3
Nanjing Maternity and Child Health Care Hospital, Nanjing 210004, China
These authors contributed equally to this work.
*
Authors to whom correspondence should be addressed.
Academic Editors: Atanas G. Atanasov, Karel Šmejkal and Elke Heiss
Received: 14 July 2016 / Revised: 3 August 2016 / Accepted: 5 August 2016 / Published: 9 August 2016
(This article belongs to the Special Issue Effects of Natural Products in the Context of Cardiometabolic Disease)
View Full-Text   |   Download PDF [2660 KB, uploaded 9 August 2016]   |  

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. View Full-Text
Keywords: salidroside; oxidative stress; nuclear factor E2-related factor 2; heme oxygenase-1; NAD(P)H dehydrogenase (quinone1); human umbilical vein endothelial cells salidroside; oxidative stress; nuclear factor E2-related factor 2; heme oxygenase-1; NAD(P)H dehydrogenase (quinone1); human umbilical vein endothelial cells
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MDPI and ACS Style

Zhu, Y.; Zhang, Y.-J.; Liu, W.-W.; Shi, A.-W.; Gu, N. Salidroside Suppresses HUVECs Cell Injury Induced by Oxidative Stress through Activating the Nrf2 Signaling Pathway. Molecules 2016, 21, 1033.

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