Cryptotanshinone inhibits TNF-α-induced early atherogenic events in vitro

J Physiol Sci. 2016 May;66(3):213-20. doi: 10.1007/s12576-015-0410-7. Epub 2016 Jan 5.

Abstract

Endothelial dysfunction has been implicated in the pathogenesis of atherosclerosis. Salvia miltiorrhiza (danshen) is a traditional Chinese medicine that has been effectively used to treat cardiovascular disease. Cryptotanshinone (CTS), a major lipophilic compound isolated from S. miltiorrhiza, has been reported to possess cardioprotective effects. However, the anti-atherogenic effects of CTS, particularly on tumor necrosis factor-α (TNF-α)-induced endothelial cell activation, are still unclear. This study aimed to determine the effect of CTS on TNF-α-induced increased endothelial permeability, monocyte adhesion, soluble intercellular adhesion molecule 1 (sICAM-1), soluble vascular cell adhesion molecule 1 (sVCAM-1), monocyte chemoattractant protein 1 (MCP-1) and impaired nitric oxide production in human umbilical vein endothelial cells (HUVECs), all of which are early events occurring in atherogenesis. We showed that CTS significantly suppressed TNF-α-induced increased endothelial permeability, monocyte adhesion, sICAM-1, sVCAM-1 and MCP-1, and restored nitric oxide production. These observations suggest that CTS possesses anti-inflammatory properties and could be a promising treatment for the prevention of cytokine-induced early atherogenesis.

Keywords: Chemokine; Cryptotanshinone; Monocyte adhesion; Nitric oxide; Soluble cellular adhesion molecule; TNF-α.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Atherosclerosis / chemically induced
  • Atherosclerosis / drug therapy*
  • Capillary Permeability / drug effects
  • Chemokine CCL2 / metabolism
  • Endothelium, Vascular / cytology
  • Endothelium, Vascular / drug effects
  • Endothelium, Vascular / metabolism
  • Human Umbilical Vein Endothelial Cells / drug effects*
  • Humans
  • In Vitro Techniques
  • Intercellular Adhesion Molecule-1 / physiology
  • Monocytes / drug effects
  • Monocytes / physiology
  • Nitric Oxide / metabolism
  • Phenanthrenes / pharmacology*
  • Tumor Necrosis Factor-alpha / antagonists & inhibitors
  • Tumor Necrosis Factor-alpha / pharmacology*
  • Vascular Cell Adhesion Molecule-1 / physiology

Substances

  • CCL2 protein, human
  • Chemokine CCL2
  • Phenanthrenes
  • Tumor Necrosis Factor-alpha
  • Vascular Cell Adhesion Molecule-1
  • Intercellular Adhesion Molecule-1
  • Nitric Oxide
  • cryptotanshinone