Objective： The aim of the study was to investigate the possible mechanism of induction apoptosis of Onychin （ONY） in ovarian cancer HO-8910 cells in vitro. Methods： Human ovarian cancer HO-8910 cells were cultured...Objective： The aim of the study was to investigate the possible mechanism of induction apoptosis of Onychin （ONY） in ovarian cancer HO-8910 cells in vitro. Methods： Human ovarian cancer HO-8910 cells were cultured in vitro. Inhibi- tory effect of ONY on the viability of HO-8910 cells was evaluated by the MTT assay. Apoptosis of HO-8910 cells treated with different concentrations of ONY for 48 h was detected by FCM. Expression of proteins related to apoptosis was analyzed by Western blot. Results： ONY significantly inhibited the viability of human ovarian cancer HO-8910 cells in a dose-dependent and time-dependent manner, and the ICso was 10.48 pg/mL for 48 h. The cells treated with ONY showed typical morphological change of apoptosis and increased cells of sub-G1 population by FCM in a dose-dependent. Western blot showed that ex- pression of Bax, cytochrome C, caspase-9 and caspase-3 proteins were upregulated and protein level of Bcl-2 was depressed after treatment with ONY in a concentration dependent. Conclusion： Apoptosis of ovarian cancer HO-8910 cells was induced by ONY through mitochondrial apoptosis pathway in vitro.展开更多
文摘Objective： The aim of the study was to investigate the possible mechanism of induction apoptosis of Onychin （ONY） in ovarian cancer HO-8910 cells in vitro. Methods： Human ovarian cancer HO-8910 cells were cultured in vitro. Inhibi- tory effect of ONY on the viability of HO-8910 cells was evaluated by the MTT assay. Apoptosis of HO-8910 cells treated with different concentrations of ONY for 48 h was detected by FCM. Expression of proteins related to apoptosis was analyzed by Western blot. Results： ONY significantly inhibited the viability of human ovarian cancer HO-8910 cells in a dose-dependent and time-dependent manner, and the ICso was 10.48 pg/mL for 48 h. The cells treated with ONY showed typical morphological change of apoptosis and increased cells of sub-G1 population by FCM in a dose-dependent. Western blot showed that ex- pression of Bax, cytochrome C, caspase-9 and caspase-3 proteins were upregulated and protein level of Bcl-2 was depressed after treatment with ONY in a concentration dependent. Conclusion： Apoptosis of ovarian cancer HO-8910 cells was induced by ONY through mitochondrial apoptosis pathway in vitro.
