作者: Jian Huang , Lijun Wu , Shin-ichi Tashiro , Satoshi Onodera , Takashi Ikejima
DOI: 10.1248/BPB.28.2068
关键词:
摘要: Drug resistance has been a major limitation to chemotherapy. There are many mechanisms that contribute such resistance. In our study, we subcloned oridonin-sensitive and low sensitive L929 cells both types of grew at almost the same growth rate. The acquired sensitivity oridonin-induced apoptosis was associated with Bcl-2 up-regulation down-regulation p53 phosphorylation. p38 inhibitor SB203580 decreased expression in made more oridonin. Moreover, higher dose oridonin promoted phosphorylation, increased Bax subsequently induced death cells, however, it had no effect on expression. Bcl-2/Bax ratio did not inhibit caspase-9 or -3 activation, but suppressed cleavage poly (ADP-ribose) polymerase (PARP), indicating existence independent PARP activation. These results indicated there relationship among oridonin, phosphorylation up-regulation.