2, 3, 5, 4′‐tetrahydroxystilbene‐2‐O‐β‐d‐glucoside protects human umbilical vein endothelial cells against lysophosphatidylcholine‐induced apoptosis by upregulating superoxide dismutase and glutathione peroxidase. Issue 10 (7th November 2014)

• Record Type: Journal Article
• Authors: Zhao, Jing; Xu, Shouzhu; Song, Fan; Nian, Lun; Zhou, Xuanxuan; Wang, Siwang
• Is Part Of: IUBMB life. Volume 66:Issue 10(2014:Oct.)
• Page Start: 711
• Page End: 722
• Publication Date: 2014-11-07
• Subjects: Biochemistry -- Periodicals; Molecular biology -- Periodicals; 572.8
• DOI: 10.1002/iub.1321
• Languages: English
• ISSNs: 1521-6543

Abstract

<abstract abstract-type="main"> <title>Abstract</title> <p>2, 3, 5, 4′‐Tetrahydroxystilbene‐2‐<italic>O</italic>‐β‐<sc>d</sc>‐glucoside (TSG) has been shown to protect human umbilical vein endothelial cells (HUVECs) from lysophosphatidylcholine (LPC)‐induced injury; however, the underlying molecular mechanism remains to be determined. The aim of this study was to investigate the protective mechanism of TSG against LPC‐induced injury in HUVECs. We established a stable LPC‐induced cell model by treating HUVECs with various concentrations of LPC and found 10.0 µg/mL of LPC to be optimal for inducing HUVECs injury. The effects of TSG on LPC‐induced cell injury were assessed by cell counting kit‐8, apoptosis assay, transmission electron microscope, and measurement of malondialdehyde (MDA), the antioxidant enzymes superoxide dismutase (SOD), reactive oxygen species (ROS), glutathione peroxidase, and mitochondrial membrane potential. The mRNA and protein levels of caspase‐3, Bax, Bcl‐2, PARP‐1, and cytochrome C were assayed by real‐time reverse transcriptase‐polymerase chain reaction and immunoblotting, respectively. TSG pretreatment was able to prevent LPC‐induced HUVECs injury and restore cell viability in a concentration‐dependent manner. LPC treated cells showed typical apoptotic morphological changes including cytoplasmic vacuolation, swollen mitochondria, and characteristic biochemical hallmarks of apoptosis including loss of mitochondrial membrane potential, activation of caspase‐3, decrease of Bcl‐2, increase of PARP‐1, upregulation of Bax, and release of cytochrome C, all of which were apparently inhibited by TSG pretreatment. Treatment of HUVECs with LPC led to decrease of SOD and glutathione peroxidase in addition to rapid increase of MDA and ROS levels. Pretreatment with TSG restored SOD and glutathione peroxidase levels to that of normal levels, and significantly decreased ROS and MDA levels. Our data indicate that TSG inhibits apoptosis of HUVECs mediated by LPC through blocking the mitochondrial apoptotic pathway and suggest that the mechanisms underlying the protective effects of TSG are related to the activation of SOD and glutathione peroxidase, the clearance of intracellular ROS, and reduction of lipid peroxidation. © 2014 IUBMB Life, 66(10):711–722, 2014</p> </abstract>