Ginsenoside Rb1 reverses H2O2-induced senescence in human umbilical endothelial cells: involvement of eNOS pathway

J Cardiovasc Pharmacol. 2012 Mar;59(3):222-30. doi: 10.1097/FJC.0b013e31823c1d34.

Abstract

Objective: Senescence of endothelial cells has been implicated in endothelial dysfunction and atherogenesis. This study investigated the effects of Rb1, a major ginsenoside in ginseng, on H2O2-induced senescence in primary human umbilical vein endothelial cells (HUVECs).

Methods and results: Real-time PCR and Western blot were used to detect the mRNA and protein expression, respectively. H2O2 (40∼100 μmol/L) effectively increased SA-β-gal activity and PAI-1 mRNA levels, two important senescence related biomarkers, in HUVECs, which were dramatically inhibited by Rb1 pre-incubation. Furthermore, Rb1 administration reversed the H2O2-decreased protein and mRNA levels of eNOS and its phosphorylation at Ser-1177, and the increased eNOS phosphorylation at Thr-495. As a result, Rb1 pretreatment restored the NO generation, as assayed by nitrate reductase method. However, pretreatment with L-NAME, a NOS inhibitor, abolished all the inhibitory effects of Rb1 on senescence. Importantly, Rb1 modulated the H2O2-altered caveolin-1 and pAkt, two most important regulators of eNOS expression and activity, in HUVECs.

Conclusions: We showed that Rb1 effectively protects HUVECs from senescence through eNOS modulation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Blotting, Western
  • Cellular Senescence / drug effects*
  • Dose-Response Relationship, Drug
  • Gene Expression Regulation / drug effects
  • Ginsenosides / pharmacology*
  • Human Umbilical Vein Endothelial Cells / drug effects
  • Human Umbilical Vein Endothelial Cells / metabolism
  • Humans
  • Hydrogen Peroxide / administration & dosage
  • Hydrogen Peroxide / toxicity
  • Nitric Oxide / metabolism*
  • Nitric Oxide Synthase Type III / genetics
  • Nitric Oxide Synthase Type III / metabolism*
  • Phosphorylation / drug effects
  • Plasminogen Activator Inhibitor 1 / genetics
  • Polymerase Chain Reaction
  • RNA, Messenger / metabolism
  • beta-Galactosidase / metabolism

Substances

  • Ginsenosides
  • Plasminogen Activator Inhibitor 1
  • RNA, Messenger
  • Nitric Oxide
  • ginsenoside Rb1
  • Hydrogen Peroxide
  • Nitric Oxide Synthase Type III
  • GLB1 protein, human
  • beta-Galactosidase