Protective effects of ginsenoside Rb1 on human umbilical vein endothelial cells in vitro.
Ginseng has beneficial effects on the cardiovascular system, but its underlying mechanism is unclear. This study investigated the effects of ginsenoside Rb1, a major constituent of ginseng, on the changes of lactate dehydrogenase (LDH) activity, nitric oxide (NO), tissue-type plasminogen activator (t-PA), and plasminogen activator inhibitor-1 (PAI-1) in oxidized low-density lipoprotein (oxLDL)-injuring endothelial cells. Human umbilical vein endothelial cells were cultured and divided into 6 groups (n = 6): control group, oxLDL alone group (100 mg/L), ginsenoside Rb1 alone group (10 microg/mL), oxLDL plus ginsenoside Rb1 groups (0.1, 1.0, and 10 microg/mL, respectively.). Twenty-four hours after treatment, LDH activity and concentrations of NO, t-PA, and PAI-1 in culture medium were measured while the expressions of endothelial nitric oxide synthase (eNOS), t-PA, and PAI-1 mRNA in endothelial cells were detected by reverse-transcriptase polymerase chain reaction. Compared with control group, oxLDL (100 mg/L) caused LDH activity, the expressions of eNOS and t-PA mRNA, and concentrations of NO and t-PA to significantly decrease (P < 0.05, respectively), and it also led to dramatic increase of PAI-1 mRNA and concentration (P < 0.05, respectively). Ginsenoside Rb1 alone did not demonstrate this ability. High-dose Rb1 (10 microg/mL) could block the effects of oxLDL on LDH activity, mRNA of eNOS, t-PA, and PAI-1, and concentrations of NO, t-PA, and PAI-1 (P < 0.05, respectively), and neither low-dose Rb1 (0.1 microg/mL) nor medium-dose Rb1 (1.0 microg/mL) demonstrated this ability. We conclude that ginsenoside Rb1 has protective effects on oxLDL-injuring human vascular endothelial cells and can reverse the effects of oxLDL on NO, t-PA, and PAI-1.
He
Fei
F
Department of Cardiology, Guangdong Provincial People's Hospital, Guangzhou, Guangdong Province, China. hefeihn@yahoo.com.cn
Guo
Rong
R
Wu
Shu-Lin
SL
Sun
Ming
M
Li
Ming
M
D004305:Dose-Response Relationship, Drug; D004730:Endothelium, Vascular / Q000187:drug effects*; D015971:Gene Expression Regulation, Enzymologic / Q000187:drug effects; D036145:Ginsenosides / Q000008:administration & dosage / Q000494:pharmacology*; D006801:Humans; D007770:L-Lactate Dehydrogenase / Q000187:drug effects / Q000378:metabolism; D008077:Lipoproteins, LDL; D009569:Nitric Oxide / Q000378:metabolism; D052250:Nitric Oxide Synthase Type III / Q000187:drug effects / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects*; D017395:Plasminogen Activator Inhibitor 1 / Q000378:metabolism; D012333:RNA, Messenger / Q000187:drug effects / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction; D010959:Tissue Plasminogen Activator / Q000187:drug effects / Q000378:metabolism; D014471:Umbilical Veins / Q000166:cytology
D036145:Ginsenosides; D008077:Lipoproteins, LDL; D017395:Plasminogen Activator Inhibitor 1; D012333:RNA, Messenger; C099252:oxidized low density lipoprotein; D009569:Nitric Oxide; C442759:ginsenoside Rb1; D007770:L-Lactate Dehydrogenase; D052250:Nitric Oxide Synthase Type III; D010959:Tissue Plasminogen Activator