Salidroside Stimulates Mitochondrial Biogenesis and Protects against H2O2-Induced Endothelial Dysfunction
Joint Authors
Li, Wenjing
Yang, Xiaoyan
Xing, Shasha
Bian, Fang
Jin, Si
Wu, Dan
Chi, Jiangyang
Xu, Gao
Zhang, Yonghui
Source
Oxidative Medicine and Cellular Longevity
Issue
Vol. 2014, Issue 2014 (31 Dec. 2014), pp.1-13, 13 p.
Publisher
Hindawi Publishing Corporation
Publication Date
2014-04-24
Country of Publication
Egypt
No. of Pages
13
Main Subjects
Abstract EN
Salidroside (SAL) is an active component of Rhodiola rosea with documented antioxidative properties.
The purpose of this study is to explore the mechanism of the protective effect of SAL on hydrogen peroxide- (H2O2-) induced endothelial dysfunction.
Pretreatment of the human umbilical vein endothelial cells (HUVECs) with SAL significantly reduced the cytotoxicity brought by H2O2.
Functional studies on the rat aortas found that SAL rescued the endothelium-dependent relaxation and reduced superoxide anion (O2∙-) production induced by H2O2.
Meanwhile, SAL pretreatment inhibited H2O2-induced nitric oxide (NO) production.
The underlying mechanisms involve the inhibition of H2O2-induced activation of endothelial nitric oxide synthase (eNOS), adenosine monophosphate-activated protein kinase (AMPK), and Akt, as well as the redox sensitive transcription factor, NF-kappa B (NF-κB).
SAL also increased mitochondrial mass and upregulated the mitochondrial biogenesis factors, peroxisome proliferator-activated receptor gamma-coactivator-1alpha (PGC-1α), and mitochondrial transcription factor A (TFAM) in the endothelial cells.
H2O2-induced mitochondrial dysfunction, as demonstrated by reduced mitochondrial membrane potential (Δψm) and ATP production, was rescued by SAL pretreatment.
Taken together, these findings implicate that SAL could protect endothelium against H2O2-induced injury via promoting mitochondrial biogenesis and function, thus preventing the overactivation of oxidative stress-related downstream signaling pathways.
American Psychological Association (APA)
Xing, Shasha& Yang, Xiaoyan& Li, Wenjing& Bian, Fang& Wu, Dan& Chi, Jiangyang…[et al.]. 2014. Salidroside Stimulates Mitochondrial Biogenesis and Protects against H2O2-Induced Endothelial Dysfunction. Oxidative Medicine and Cellular Longevity،Vol. 2014, no. 2014, pp.1-13.
https://search.emarefa.net/detail/BIM-1047159
Modern Language Association (MLA)
Xing, Shasha…[et al.]. Salidroside Stimulates Mitochondrial Biogenesis and Protects against H2O2-Induced Endothelial Dysfunction. Oxidative Medicine and Cellular Longevity No. 2014 (Dec. 2014), pp.1-13.
https://search.emarefa.net/detail/BIM-1047159
American Medical Association (AMA)
Xing, Shasha& Yang, Xiaoyan& Li, Wenjing& Bian, Fang& Wu, Dan& Chi, Jiangyang…[et al.]. Salidroside Stimulates Mitochondrial Biogenesis and Protects against H2O2-Induced Endothelial Dysfunction. Oxidative Medicine and Cellular Longevity. 2014. Vol. 2014, no. 2014, pp.1-13.
https://search.emarefa.net/detail/BIM-1047159
Data Type
Journal Articles
Language
English
Notes
Includes bibliographical references
Record ID
BIM-1047159