ABSTRACT
Aim Toexploretheinhibitioneffectof triptolide on nasopharynx cancer, and the mechanism. Methods Theinhibitionofcellproliferationwasde-tected by MTT assay;the cell apoptosis was analyzed by flow cytometry with propidium iodide staining. The ex-pressions of glucose regulated protein 78 ( GRP-78 ) , Akt and pAkt in cells were examined by Western blot;the effect of triptolide on reactive oxygen species ( ROS) accumulation was detected by ROS Fluorescent Probe-DHE.Results MTTassayshowedthatthe growth of nasopharynx cancer was inhibited by triptol-ide , and the inhibition occurred in a dose and time-de-pendent manner following triptolide treatment in CNE-2Z nasopharynx cancer cells. Propidium iodide staining revealed that the apoptosis of CNE-2 Z cells was in-duced remarkably by triptolide. After CNE-2Z cells treated with 25, 50,100 nmol·L-1 of triptolide for 24 h, the apoptosis rate was 14%,26. 9% and 34. 4% re-spectively. Western blot experiment showed that the expression of GRP-78 had no significant change follow-ing triptolide treatment in CNE-2 Z nasopharynx cancer cells for 24 h, but the expression and the phosphoryla-tion level of Akt were strikingly decreased. The experi-ment of ROS uncovered that CNE-2 Z nasopharynx cancer cells increased generation of ROS after treat-ment with triptolide for 4 hours, and acted cells in a dosedependentmanner.Conclusions Triptolidecan inhibit the growth of CNE-2 Z nasopharynx cancer cells in a dose and time-dependent maner. The mechanism may be related with the point that triptolide can induce oxidative stress, incease ROS, inhibit the expression and the phosphorylation level of Akt,then promote the apoptosis of CNE-2Z cells.