Objective:To investigate the mechanism by which hydroxyl safflower yellow A,an active component of safflower (Carthamus tinctorius L.),promotes apoptosis in abnormal human umbilical vein endothelial cells (HUVECs).Met...Objective:To investigate the mechanism by which hydroxyl safflower yellow A,an active component of safflower (Carthamus tinctorius L.),promotes apoptosis in abnormal human umbilical vein endothelial cells (HUVECs).Methods:Supernatant of BGC-823 was used to stimulate HUVECs to establish a model of abnormal proliferation of HUVECs.After determining an ideal concentration of HSYA by MTT assay,apoptosis was detected with flow cytometry and TUNEL assay.Mechanism of apoptosis was assessed using quantitative real-time polymerase chain reaction,Western blot,and ELISA.Results:A range of concentrations of HSYA inhibited proliferation and promoted apoptosis of abnormal HUVECs.As the rate of apoptosis increased,mRNA expression of caspase-3 increased while expression of mutant p53 decreased.HSYA had no effect on Fas gene expression.Analogously,protein expression of Bax was increased while those of Bcl-2,Fas,and Fas-L were decreased.Conclusions:HSYA appears to induce apoptosis of HUVECs with the stimulation of the supematant of tumor cells.The mechanism of apoptosis by HSYA may involve activation of the mitochondrial apoptotic pathway and regulation of the expressions of Bcl-2,Bax,and p53.展开更多
文摘Objective:To investigate the mechanism by which hydroxyl safflower yellow A,an active component of safflower (Carthamus tinctorius L.),promotes apoptosis in abnormal human umbilical vein endothelial cells (HUVECs).Methods:Supernatant of BGC-823 was used to stimulate HUVECs to establish a model of abnormal proliferation of HUVECs.After determining an ideal concentration of HSYA by MTT assay,apoptosis was detected with flow cytometry and TUNEL assay.Mechanism of apoptosis was assessed using quantitative real-time polymerase chain reaction,Western blot,and ELISA.Results:A range of concentrations of HSYA inhibited proliferation and promoted apoptosis of abnormal HUVECs.As the rate of apoptosis increased,mRNA expression of caspase-3 increased while expression of mutant p53 decreased.HSYA had no effect on Fas gene expression.Analogously,protein expression of Bax was increased while those of Bcl-2,Fas,and Fas-L were decreased.Conclusions:HSYA appears to induce apoptosis of HUVECs with the stimulation of the supematant of tumor cells.The mechanism of apoptosis by HSYA may involve activation of the mitochondrial apoptotic pathway and regulation of the expressions of Bcl-2,Bax,and p53.
