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Salidroside Suppresses HUVECs Cell Injury Induced by Oxidative Stress through Activating the Nrf2 Signaling Pathway.
Molecules. 2016 Aug 09; 21(8)M

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+Show Affiliations

First College of Clinical Medicine, Nanjing University of Traditional Chinese Medicine, Nanjing 210023, China. zy_njtcm@126.com.Nanjing Hospital of Traditional Chinese Medicine, Nanjing 210001, China. zhangyajie_jack@126.com.First College of Clinical Medicine, Nanjing University of Traditional Chinese Medicine, Nanjing 210023, China. cheeseweiweiliu@126.com.Nanjing Maternity and Child Health Care Hospital, Nanjing 210004, China. shiaiwu888@163.com.Nanjing Hospital of Traditional Chinese Medicine, Nanjing 210001, China. jsguning@163.com.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

27517893

Citation

Zhu, Yao, et al. "Salidroside Suppresses HUVECs Cell Injury Induced By Oxidative Stress Through Activating the Nrf2 Signaling Pathway." Molecules (Basel, Switzerland), vol. 21, no. 8, 2016.
Zhu Y, Zhang YJ, Liu WW, et al. Salidroside Suppresses HUVECs Cell Injury Induced by Oxidative Stress through Activating the Nrf2 Signaling Pathway. Molecules. 2016;21(8).
Zhu, Y., Zhang, Y. J., Liu, W. W., Shi, A. W., & Gu, N. (2016). Salidroside Suppresses HUVECs Cell Injury Induced by Oxidative Stress through Activating the Nrf2 Signaling Pathway. Molecules (Basel, Switzerland), 21(8). https://doi.org/10.3390/molecules21081033
Zhu Y, et al. Salidroside Suppresses HUVECs Cell Injury Induced By Oxidative Stress Through Activating the Nrf2 Signaling Pathway. Molecules. 2016 Aug 9;21(8) PubMed PMID: 27517893.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Salidroside Suppresses HUVECs Cell Injury Induced by Oxidative Stress through Activating the Nrf2 Signaling Pathway. AU - Zhu,Yao, AU - Zhang,Ya-Jie, AU - Liu,Wei-Wei, AU - Shi,Ai-Wu, AU - Gu,Ning, Y1 - 2016/08/09/ PY - 2016/07/14/received PY - 2016/08/03/revised PY - 2016/08/05/accepted PY - 2016/8/13/entrez PY - 2016/8/16/pubmed PY - 2017/4/18/medline KW - NAD(P)H dehydrogenase (quinone1) KW - heme oxygenase-1 KW - human umbilical vein endothelial cells KW - nuclear factor E2-related factor 2 KW - oxidative stress KW - salidroside JF - Molecules (Basel, Switzerland) JO - Molecules VL - 21 IS - 8 N2 - 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. SN - 1420-3049 UR - https://www.unboundmedicine.com/medline/citation/27517893/Salidroside_Suppresses_HUVECs_Cell_Injury_Induced_by_Oxidative_Stress_through_Activating_the_Nrf2_Signaling_Pathway_ L2 - https://www.mdpi.com/resolver?pii=molecules21081033 DB - PRIME DP - Unbound Medicine ER -