蜂斗菜素诱导骨髓瘤RPMI 8226细胞凋亡及其机制.

Objective To investigate the apoptotic effect of petasin on myeloma RPMI 8226 cells and the mechanisms. Methods The inhibition of petasin on the proliferation of myeloma RPMI 8226 cells was tested by trypan blue assay. Apoptosis of RPMI 8226 cells was measured by terminal-deoxynueleotidyl transferase mediated dUTP nick end labeling (TUNEL) assay and Hoechst 33258 staining assay. Effects of petasin on caspase-3, 8 and 9 expressions, phosphorylation of ERK1/2, MEK(p-ERK1/2; p-MEK) and p38MAPK(p-p38MAPK) protein were analyzed by Western blot. Results Incubation by petasin for 24h, 48h or 72h could significantly inhibit the proliferation of myeloma RPMI 8226 cells (P<0.01, P<0.01, P<0.01). Petasin induced the apoptosis of myeloma RPMI 8226 cells in time- and concentration-dependent manners (P<0.05, P<0.05). Caspase inhibitor pretreatment could significantly inhibit the apoptosis of myeloma cells. After cultured with petasin for 72h, the expressions of caspase-3, 8 and 9 were obviously enhanced (P<0.05, P<0.01, P<0.05) and phosphorylation of p-p38MAPK of RPMI8226 cells was significantly increased (P<0.01). However, phosphorylation of p-ERK1/2 and p-MEK was decreased significantly (P<0.01, P<0.05). Conclusion Petasin can inhibit the proliferation of myeloma RPMI 8226 cells and induce apoptosis. The mechanism may be related to the activation of caspase-3, 8 and 9 proteins and the changes in phosphorylation of p38MAPK, ERK1/2 and MEK. [ABSTRACT FROM AUTHOR]