Ophiopogonin D prevents H2O2-induced injury in primary human umbilical vein endothelial cells

J Ethnopharmacol. 2010 Mar 24;128(2):438-45. doi: 10.1016/j.jep.2010.01.031. Epub 2010 Jan 18.

Abstract

Aim of the study: Vessel endothelium injury caused by reactive oxygen species (ROS) including H(2)O(2) plays a critical role in the pathogenesis of cardiovascular disorders. Therefore, drug targeting ROS elimination has highly clinical values in cardiovascular therapy. The plant of Radix Ophiopogon japonicus is a traditional Chinese herbal medicine that has been commonly used for prevention and treatment of cardiovascular diseases for a long history. However, the effective component mediating its beneficial effects remains unknown. In the present study, we investigated the action of Ophiopogonin D (OP-D), one of the most bioactive components of Radix Ophiopogon japonicus, in an endothelial injury model induced by H(2)O(2).

Materials and methods: Primarily cultured human umbilical vein endothelial cells (HUVECs) were pretreated with increased doses of OP-D overnight and then challenged with H(2)O(2). The protective effects of OP-D against H(2)O(2) were evaluated.

Results: We found that OP-D inhibited mRNA levels of antioxidant, inflammatory and apoptotic genes in a dose-dependent manner in HUVECs. H(2)O(2)-induced lipid peroxidation and protein carbonylation were reduced by OP-D pretreatment. Mitochondrial ROS generation and cell apoptosis were also attenuated in OP-D pretreated cells. In addition, OP-D restored cellular total antioxidative capacity and inhibited the release of inflammatory cytokines. Furthermore, OP-D suppressed the enzymatic activity of catalase, HO-1, and caspases. Finally, OP-D blocked activation of NF-kappaB and ERK signaling cascades.

Conclusion: Our findings provide the first evidence that OP-D plays a protective role as an effective antioxidant in H(2)O(2)-induced endothelial injury. Ophiopogonin D can be therefore developed as a novel drug for the therapy of cardiovascular disorders.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antioxidants / metabolism
  • Apoptosis / drug effects
  • Caspases / metabolism
  • Cells, Cultured
  • Endothelial Cells / drug effects*
  • Endothelial Cells / metabolism
  • Endothelium / metabolism
  • Humans
  • Hydrogen Peroxide / pharmacology*
  • Lipid Peroxidation / drug effects
  • Mitochondria / metabolism
  • NF-kappa B / metabolism
  • Nitric Oxide Synthase Type III / metabolism
  • Reactive Oxygen Species / metabolism
  • Saponins / pharmacology*
  • Signal Transduction / drug effects
  • Spirostans / pharmacology*
  • Umbilical Veins / metabolism*

Substances

  • Antioxidants
  • NF-kappa B
  • Reactive Oxygen Species
  • Saponins
  • Spirostans
  • ophiopogonin D
  • Hydrogen Peroxide
  • NOS3 protein, human
  • Nitric Oxide Synthase Type III
  • Caspases