Triptolide: a potent inhibitor of NF-kappa B in T-lymphocytes
Abstract
"AIM:
To study the effect of triptolide on the activity of nuclear factor-kappa B (NF-kappa B) and gene expression of I kappa B alpha, a major inhibitor of NF-kappa B, in human Jurkat T cell line.
METHODS:
Jurkat cells treated with or without PMA/PHA were incubated with varied doses of triptolide for different time periods. The activity of NF-kappa B in Jurkat cells was measured with electrophoretic mobility shift assays (EMSA), and the mRNA expression of I kappa B alpha in Jurkat cells was detected by semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR).
RESULTS:
PMA/PHA treatment was found to induce NF-kappa B activation rapidly. Triptolide treatment decreased the activity of NF-kappa B in both PMA/PHA treated and untreated Jurkat cells. This effect of triptolide was in a dose-dependent manner and was more obvious in cells treated with PMA/PHA. The mRNA expression of I kappa B alpha were upregulated by triptolide, while this effect was more potent in cells without PMA/PHA treatment.
CONCLUSION:
Triptolide is a potent inhibitor of NF-kappa B activation in T lymphocyte and this effect is partly due to the upregulation of I kappa B alpha mRNA expression."
Keywords:
To study the effect of triptolide on the activity of nuclear factor-kappa B (NF-kappa B) and gene expression of I kappa B alpha, a major inhibitor of NF-kappa B, in human Jurkat T cell line.
METHODS:
Jurkat cells treated with or without PMA/PHA were incubated with varied doses of triptolide for different time periods. The activity of NF-kappa B in Jurkat cells was measured with electrophoretic mobility shift assays (EMSA), and the mRNA expression of I kappa B alpha in Jurkat cells was detected by semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR).
RESULTS:
PMA/PHA treatment was found to induce NF-kappa B activation rapidly. Triptolide treatment decreased the activity of NF-kappa B in both PMA/PHA treated and untreated Jurkat cells. This effect of triptolide was in a dose-dependent manner and was more obvious in cells treated with PMA/PHA. The mRNA expression of I kappa B alpha were upregulated by triptolide, while this effect was more potent in cells without PMA/PHA treatment.
CONCLUSION:
Triptolide is a potent inhibitor of NF-kappa B activation in T lymphocyte and this effect is partly due to the upregulation of I kappa B alpha mRNA expression."