
pmid: 11516264
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.
Flavonoids, Flavonols, T-Lymphocytes, Apoptosis, Lymphocyte Activation, Antioxidants, Jurkat Cells, Cyclosporine, Humans, Interleukin-2, Drug Interactions, Phytohemagglutinins
Flavonoids, Flavonols, T-Lymphocytes, Apoptosis, Lymphocyte Activation, Antioxidants, Jurkat Cells, Cyclosporine, Humans, Interleukin-2, Drug Interactions, Phytohemagglutinins
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