Salidroside Stimulates Mitochondrial Biogenesis and Protects against H2O2-Induced Endothelial Dysfunction. (24th April 2014)

• Record Type: Journal Article
• Authors: Xing, Shasha; Yang, Xiaoyan; Li, Wenjing; Bian, Fang; Wu, Dan; Chi, Jiangyang; Xu, Gao; Zhang, Yonghui; Jin, Si
• Other Names: Deng Shiwei Academic Editor.
• Is Part Of: Oxidative medicine and cellular longevity. Volume 2014(2014)
• Publication Date: 2014-04-24
• Subjects: Oxidative stress -- Periodicals; Cells -- Aging -- Periodicals; Cells -- Aging; Oxidative stress; Oxidative Stress -- Periodicals; Cell Aging -- Periodicals; Periodicals; 611.0181
• DOI: 10.1155/2014/904834
• Languages: English
• ISSNs: 1942-0900

Abstract

Abstract : 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- (H2 O2 -) induced endothelial dysfunction. Pretreatment of the human umbilical vein endothelial cells (HUVECs) with SAL significantly reduced the cytotoxicity brought by H2 O2 . Functional studies on the rat aortas found that SAL rescued the endothelium-dependent relaxation and reduced superoxide anion (O 2 ∙ - ) production induced by H2 O2 . Meanwhile, SAL pretreatment inhibited H2 O2 -induced nitric oxide (NO) production. The underlying mechanisms involve the inhibition of H2 O2 -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- κ B). SAL also increased mitochondrial mass and upregulated the mitochondrial biogenesis factors, peroxisome proliferator-activated receptor gamma-coactivator-1alpha (PGC-1 α ), and mitochondrial transcription factor A (TFAM) in the endothelial cells. H2 O2 -induced mitochondrial dysfunction, as demonstrated by reduced mitochondrial membrane potential (Δ ψ m) and ATP production, was rescued by SAL pretreatment. Taken together, these findings implicate that SAL could protect endothelium against H2 O2 -induced injury via promoting mitochondrial biogenesis and function, thus preventing the overactivation of oxidative stress-related downstream signaling pathways.