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The Role Of Ginsenoside-Rg1 In Ox-LDL Induced Human Umbilical Vein Endothelial Cell Inflammation

Posted on:2017-05-24Degree:MasterType:Thesis
Country:ChinaCandidate:J S GuFull Text:PDF
GTID:2284330488497909Subject:Internal Medicine
Abstract/Summary:PDF Full Text Request
Objective:The study was designed to investigate the protective effects of ginsenoside-Rgl on oxidized low-density lipoprotein induced human umbilical vein endothelial cell inflammation.Methods:HUVECs were cultured and treated differently in vitro and randomly divided into following groups, including the blank control group, the ox-LDL induced(2,6,12 and 24h) group, ginsenoside-Rgl (5,10,20 and 50 μmol/L) treatment group and 10μmol/L Rg1 with 5μmol/L PD98059 treatment group,etc. The variation of protein expression levels of vascular cell adhesion molecule-1 (VCAM-1),intercelluar adhesion molecule-1 (ICAM-1),nuclear factor-κB (NF-κB) and extracellular signal-regulated kinase 1/2 (ERK1/2) of MAP kinase signaling system were measured by western blotting.The intracellular reactive oxygen species (ROS) was detected by 2’,7’-dichlorofluorescein diacetate (DCFH-DA).Results:50μg/mL Ox-LDL showed significantly time-independent promotion on he protein expression levels of VCAM-1 and ICAM-1 in HUVECs within 24 hours; ROS production and NF-κB activation were also time-independent which had a peak at 24 hours.10μg/mL ginsenoside-Rgl inhibited VCAM-1 and ICAM-1 expression and ROS production in ox-LDL induced HUVECs.Adding ERK1/2 inhibitor PD98059, Iκ-B expression further increased but VCAM-1 and ICAM-1 expression further decreased.Conclusion:This report demonstrates that ginsenoside-Rgl shows critical protection on ox-LDL induced HUVECs inflammation.This effect is not only by decreasing ROS production,but also by suppressing VCAM-1 and ICAM-1 expression via inhibition of ERK/NF-κB pathway.
Keywords/Search Tags:ginsenoside-Rgl, atherosclerosis, cell adhesion molecule, reactive oxygen species, MAP kinase signaling system
PDF Full Text Request
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