Effect of safrole oxide on vascular endothelial cell growth and apoptosis induced by deprivation of fibroblast growth factor.
Abstract
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.
Keywords:
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.