The inhibitory effect of parthenolide combined with adriamycin on proliferation of leukemia Jurkat cells

WANG Xiaotao; LIU Ling; TANG Ailin; HE Yuchan

Abstract：Objective To investigate the inhibitory effect of parthenolide(PTL) combined with adriamycin (ADM)on prolifera-tion and apoptosis of adult acute T lymphoblastic leukemia Jurkat cells and their possible mechanism. Methods MTT assay was applied to calculate the half inhibitory concentration(IC50) of PTL and ADM for 48h, and detect the inhibition rates by treating Jurkat cells with different concentration groups of PTL(4,8,16μmol/L) or ADM (0?25,0?5,1μmol/L) for 48h. Flow cytometry was applied to detect the apoptosis rate by treating Jurkat cells with ADM (0?25, 0?5, 1μmol/L), PTL (4, 8, 16μmol/L), and PTL (8μmol/L) combined with ADM (0?5μmol/L) for 48h. Immunohistochemical method was employed to detect the expression of protein nuclear factor-κBp65 (NF-κBp65) treated by ADM (0?5μmol/L), PTL (8μmol/L), and PTL (8μmol/L) combined with ADM (0?5μmol/L). Blank control group was set for above experiments. Results MTT assay showed that PTL and ADM inhibited the growth of Jurkat cells in a dose-de-pendent manner, with IC50 of 8?11μmol/L and 0?53μmol/L at 48h. Compared with single drug groups and control group, PLT combined with ADM could significantly inhibit the proliferation of Jurkat cells. Flow cytometry showed that the apoptosis rate of Jurkat cells in PTL or ADM single agent group was in a dose-dependent manner. The apoptosis rate of combined group was (84?50±5?64) %, higher than those of single agent groups and control group ( P<0?05) . Immunohistochemical detection showed that the positive score of NF-κBp65 in PTL and PTL combined with ADM was lower than control group (P<0?05), while in ADM group was higher than control group (P<0?05), and the combined group was lower than the two single agent groups (P<0?05). Conclusion PTL may inhibit the expression of NF-κBp65 protein, raise the ability of inhibition of ADM on Jurkat cells proliferation, and promote cells apoptosis.