Abstract: Objective To investigate the molecular mechanisms by which triptolide induces apoptosis of human acute T
lymphocytic leukemia Jurkat cells. Methods MTT assay was employed to detect the proliferation inhibition of Jurkat cells by
triptolide, and the IC50 was calculated by OriginPro8. Flow cytometry was used to analyze apoptosis of Jurkat cells. Np9
mRNA levels were detected by RT-PCR and analyzed quantitatively by Kodak 1D 3.6 software. Correlation between the
inhibition of Np9 transcription and the cell apoptosis was analyzed by SPSS 19.0.Western blotting was employed to determine
Np9 downstream signaling molecules c-myc, β-catenin, ERK, AKT and Notch1 protein level in Jurkat cells after exposure to
different concentrations of triptolide for 48h. Results Triptolide treatment resulted in dose-dependent inhibition of Jurkat cells
proliferation and its IC50 was 12.7nmol/L. Triptolide induced apoptosis of Jurkat cells in dose- dependent manner. Furthermore,
triptolide inhibited Np9 mRNA transcription level in Jurakt cells in a dose-dependent manner. There was a correlation
between the triptolide-mediated the apoptosis and the inhibition of Np9 transcription of Jurkat cells (R2=0.907). Western
blotting results displayed that triptolide inhibited transcription levels of Np9 mRNA with a concomitant decrease of its
downstream signaling molecules c-myc, β-catenin, ERK, AKT and Notch1 at protein levels. Conclusion Inhibition of HERV-K
Np9 mRNA and its downstream signaling molecules c-myc, β-catenin, ERK, Akt and Notch1 protein might be one of
important molecular mechanisms by which triptolide induces apoptosis of human acute T lymphocytic leukemia Jurkat cells.