title: Protective effects of ginsenoside Rb1 on human umbilical vein endothelial cells in vitro.
abstract: 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.
authors: Department of Cardiology, Guangdong Provincial People's Hospital, Guangzhou, Guangdong Province, China. hefeihn@yahoo.com.cn
authors: Fei
authors: F
authors: He
authors: Rong
authors: R
authors: Guo
authors: Shu-Lin
authors: SL
authors: Wu
authors: Ming
authors: M
authors: Sun
authors: Ming
authors: M
authors: Li
mesh_terms: 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
chemical_list: 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