Ponicidin (Rubescensine B) is a diterpenoid derived from Rabdosia rubescens that exhibits immunoregulatory, anti-inflammatory, anti-viral, and anti-cancer activity. Ponicidin induces apoptosis of gastric carcinoma cells, decreases the phosphorylation of JAK2 and STAT3, and shows no effect on the protein levels of JAK2 and STAT3.

K562 cells in culture medium in vitro were given different concentrations of Ponicidin (10-50 micromol x L(-1)) for 24, 48, and 72 h. The inhibitory rate of the cells was measured by MTT assay, cell apoptotic rates were detected by flow cytometry (FCM) using Annexin V staining after K562 cells were treated with different concentrations of Ponicidin for 72 hours, and cell morphology was observed by Wright-Giemsa staining. Ponicidin (over 30 micromol x L(-1)) could inhibit the growth of K562 cells in both time- and dose-dependent manner. FCM analysis revealed that apoptotic cells were gradually increased in a dose-dependent manner after treatment for 72 hours, and that marked morphological changes of cell apoptosis such as condensation of chromatin was clearly observed by Wright-Giemsa staining after treatment by 50 micromol x L(-1) Ponicidin. Furthermore, Western blotting also showed that expression of p-AKT and p-P85 in PI3K/AKT signaling pathways was downregulated dramatically whereas the expression of p-P38, as well as p-ERK and p-JNK, remained unchanged after the cells were treated by PON for 48 h.