AIM: To investigate effect of safrole oxide on cell growth and apoptosis induced by deprivation of survival factors (fibroblast growth factors, aFGF and bFGF) in vascular endothelial cells (VEC). METHODS: Morphological changes were observed by light microscopy. Cell growth was determined by MTT (3-[4, 5-dimethylthiazol-2-yl]-2, 5-diphenyltetrazolium) method. DNA fragmentation was analyzed by agarose gel electrophoresis and fluorescence microscopy. Cell cycle distribution was analyzed by flow cytometry (FCM). RESULTS: The cells deprived of FGF were exposed to safrole oxide 5-25 mg/L for 24 h. Cells spreading and growth were promoted (P<0.01), detachment and DNA fragmentation of these cells were suppressed (P<0.01), safrole oxide 10 mg/L had no obvious effect on cell cycle distribution (P>0.05). When the cells were treated with safrole oxide 50-100 mg/L, detachment and DNA fragmentation of VEC were promoted (P<0.01). The cell cycle was blocked at G2-M phase by safrole oxide 100 mg/L. CONCLUSION: Safrole oxide 10 mg/L inhibited, but 100 mg/L promoted apoptosis of VEC. Safrole oxide might be an important compound that affects VEC growth and apoptosis.
AIM: To investigate effect of safrole oxide on cell growth and apoptosis induced by deprivation of survival factors (fibroblast growth factors, aFGF and bFGF) in vascular endothelial cells (VEC). METHODS: Morphological changes were observed by light microscopy. Cell growth was determined by MTT (3-[4, 5-dimethylthiazol-2-yl]-2, 5-diphenyltetrazolium) method. DNA fragmentation was analyzed by agarose gel electrophoresis and fluorescence microscopy. Cell cycle distribution was analyzed by flow cytometry (FCM). RESULTS: The cells deprived of FGF were exposed to safrole oxide 5-25 mg/L for 24 h. Cells spreading and growth were promoted (P<0.01), detachment and DNA fragmentation of these cells were suppressed (P<0.01), safrole oxide 10 mg/L had no obvious effect on cell cycle distribution (P>0.05). When the cells were treated with safrole oxide 50-100 mg/L, detachment and DNA fragmentation of VEC were promoted (P<0.01). The cell cycle was blocked at G2-M phase by safrole oxide 100 mg/L. CONCLUSION:Safrole oxide 10 mg/L inhibited, but 100 mg/L promoted apoptosis of VEC. Safrole oxide might be an important compound that affects VEC growth and apoptosis.