Astilbin Selectively Facilitates the Apoptosis of interleukin-2-dependent Phytohemagglutinin-Activated Jurkat Cells

Pharmacol Res. 2001 Aug;44(2):135-9. doi: 10.1006/phrs.2001.0838.


The present study examined the relationship between the activation of T cells and the apoptosis-facilitating effect of astilbin on them. By the stimulation of PHA, a remarkable IL-2 production was detected in the supernatant of Jurkat cells after 120 h among 72--144 h incubation. This kinetics was quite in accordance with that of astilbin-induced apoptosis of Jurkat cells, where 1 h-exposure of the PHA-activated cells to astilbin caused a significantly increased apoptosis in a dose-dependent manner. To the Jurkat cells that had been cultivated for 72--144 h without PHA, however, astilbin did not show any facilitation of the cell apoptosis. Pre-treatment by cyclosporine A simultaneously with PHA dose-dependently lowered the IL-2 production and susceptibility of the cells to astilbin, while the treatment after 120 h of PHA-activation did not. The exogenous IL-2 treatment after 72 h of PHA-activation significantly and dose-dependently raised the susceptibility of the Jurkat cells to astilbin. These results indicated the dependency of the apoptosis-facilitating effect of astilbin on appropriate status of activated T lymphocytes with a relation to IL-2 production. This characteristic of astilbin may be of great significance for the treatment of a variety of immunologically related diseases.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antioxidants / pharmacology
  • Apoptosis*
  • Cyclosporine / pharmacology
  • Drug Interactions
  • Flavonoids / pharmacology*
  • Flavonols*
  • Humans
  • Interleukin-2 / metabolism*
  • Jurkat Cells
  • Lymphocyte Activation / drug effects*
  • Phytohemagglutinins / pharmacology*
  • T-Lymphocytes / drug effects*
  • T-Lymphocytes / pathology


  • Antioxidants
  • Flavonoids
  • Flavonols
  • Interleukin-2
  • Phytohemagglutinins
  • astilbin
  • Cyclosporine