[Effect of ASO Blood Stasis Syndrome Serum on Vascular Endothelial Cell Injury and Regulation of Taohong Siwu Decoction on it]

Zhongguo Zhong Xi Yi Jie He Za Zhi. 2015 Nov;35(11):1373-7.
[Article in Chinese]

Abstract

Objective: To explore the effect of arteriosclerosis obliterans (ASO) blood stasis syndrome (BSS) serum on vascular endothelial cell injury and to study the regulation of Taohong Siwu Decoction (TSD) on it.

Methods: Umbilical vein endothelial cell culture system was established. The serum endothelial cell injury model with ASO BSS was prepared. Low, medium, and high concentrations TSD containing serums were respectively added. The endothelial cell proliferation activity was observed by MTT method. Ultrastructures of endothelial cells were observed under transmission electron microscope. Changes of intracellular calcium ion concentration and the cytoskeleton were observed under laser confocal microscope. Contents of ET, NO, and transforming growth factor beta1 (TGF-beta1) in endothelial cell culture supernatant were detected by ELISA.

Results: In ASO BSS serum group endothelial cell proliferation activities decreased, the cell structure was obviously destroyed, calcium ion concentration increased, contents of ET, NO and TGF-beta1 increased significantly (P < 0.01), and ET/NO ratio was imbalanced. After incubating with TSD drug containing serum, endothelial cell proliferation activities and injured cell structures were obviously improved; ET, NO and TGF-beta1 levels decreased (P < 0.05, P < 0.01), ET/NO ratios approximated to the normal level.

Conclusion: The main mechanism of TSD for treating ASO ASS lied in improving injured vascular endothelial cells and endocrine disorder.

MeSH terms

  • Arteriosclerosis Obliterans*
  • Cell Proliferation
  • Drugs, Chinese Herbal / therapeutic use*
  • Endothelial Cells
  • Humans
  • Medicine, Chinese Traditional*
  • Serum
  • Transforming Growth Factor beta1 / metabolism
  • Umbilical Veins

Substances

  • Drugs, Chinese Herbal
  • Transforming Growth Factor beta1