Hydroxysafflor yellow B induces apoptosis via mitochondrial pathway in human gastric cancer cells

Abstract

Abstract Objectives Hydroxysafflor yellow B (HSYB) is extracted from the petals of the safflower, a Chinese medicine. Relevant research results have demonstrated that HSYA can suppress the abnormal tumour cell proliferation and induce cell apoptosis. However, the properties of HSYB have rarely been reported, especially its antitumour effects on gastric cancer (GC). Methods SGC-7901 and BGC-823 cells were treated with different concentrations of HSYB. Cell proliferation inhibition rate was detected by 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and colony formation detection. The changes in morphology of cells was observed by Hoechst 33258 staining. Cell apoptosis was evaluated by Annexin V-FITC/PI (fluoresceinisothiocyanate/propidium iodide) double staining. JC-1 was used to detect the level of mitochondrial membrane potential (MMP). The protein levels of cleaved-caspase-3, cleaved-caspase-9, APAF-1, cytoplasmic cytochrome C, BAX and BCL-2 were examined by western blot. Key findings HSYB significantly suppressed the proliferation of SGC-7901 and BGC-823 cells. Hoechst 33258 staining assay showed that HSYB treatment triggered apoptotic morphology and the apoptotic rates were significantly increased after being treated with HSYB and the mitochondrial membrane potential was gradually decreased in human GC cells. In addition, Western blot analysis revealed that the levels of cleaved-caspase-3 and cleaved-caspase-9 were remarkably increased in HSYB-treated BGC-823 and SGC-7901 cells. And, the levels of apoptotic protease activating factor-1 (APAF-1) and cytoplasmic cytochrome C were remarkably up-regulated in HSYB-treated cells. At the same time, HSYB could up-regulate the level of BAX and down-regulate the level of BCL-2. Conclusions Our data suggest that HSYB could induce GC cell apoptosis via the mitochondrial pathway.