Glossogyne tenuifolia Extract Inhibits TNF-α-Induced Expression of Adhesion Molecules in Human Umbilical Vein Endothelial Cells via Blocking the NF-kB Signaling Pathway

Molecules. 2015 Sep 17;20(9):16908-23. doi: 10.3390/molecules200916908.

Abstract

Chronic inflammation plays a pivotal role in the development of atherosclerosis, where the pro-inflammatory cytokine-induced expression of endothelial adhesion molecules and the recruitment of monocytes are the crucial events leading to its pathogenesis. Glossogyne tenuifolia ethanol extract (GTE) is shown to have potent anti-inflammatory and antioxidant activities. We evaluated the effects of GTE and its major components, luteolin (lut), luteolin-7-glucoside (lut-7-g), and oleanolic acid (OA) on TNF-α-induced expression of adhesion molecules in human umbilical vein endothelial cells (HUVECs). The results demonstrated that GTE, lut, and lut-7-g attenuated the expression of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) in TNF-α-activated HUVECs, and inhibited the adhesion of monocytes to TNF-α-activated HUVECs. The TNF-α-induced mRNA expression of ICAM-1 and VCAM-1 was also suppressed, revealing their inhibitory effects at the transcriptional level. Furthermore, GTE, lut, and lut-7-g blocked the TNF-α-induced degradation of nuclear factor-kB inhibitor (IkB), an indicator of the activation of nuclear factor-kB (NF-kB). In summary, GTE and its bioactive components were effective in preventing the adhesion of monocytes to cytokine-activated endothelium by the inhibition of expression of adhesion molecules, which in turn is mediated through blocking the activation and nuclear translocation of NF-kB. The current results reveal the therapeutic potential of GTE in atherosclerosis.

Keywords: Glossogyne tenuifolia; adhesion molecule; luteolin; luteolin-7-glucoside; nuclear factor-kB.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Asteraceae / chemistry*
  • Cell Adhesion / drug effects
  • Chemokines / genetics*
  • Chemokines, CXC
  • Endothelial Cells / drug effects*
  • Endothelial Cells / metabolism
  • Glucosides / pharmacology
  • Human Umbilical Vein Endothelial Cells
  • Humans
  • Intercellular Adhesion Molecule-1 / genetics*
  • Luteolin / pharmacology
  • NF-kappa B
  • Oleanolic Acid / pharmacology
  • Plant Extracts / chemistry
  • Plant Extracts / pharmacology*
  • Signal Transduction / drug effects
  • Tumor Necrosis Factor-alpha / pharmacology*

Substances

  • CXCL17 protein, human
  • Chemokines
  • Chemokines, CXC
  • Glucosides
  • NF-kappa B
  • Plant Extracts
  • TNF protein, human
  • Tumor Necrosis Factor-alpha
  • Intercellular Adhesion Molecule-1
  • Oleanolic Acid
  • luteolin-7-glucoside
  • Luteolin