AIM: To investigate the signaling pathways implicated in phosphatidylethanolamine (PE)-induced apoptosis of human hepatoma HepG2 cells. METHODS: Inhibitory effects of PE on human hepatoma HepG2 cells were detected by ...AIM: To investigate the signaling pathways implicated in phosphatidylethanolamine (PE)-induced apoptosis of human hepatoma HepG2 cells. METHODS: Inhibitory effects of PE on human hepatoma HepG2 cells were detected by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Cell cycle, apoptosis and mitochondrial transmembrane potential (ΔΨm) were analyzed by flow cytometry. Immunocytochemical assay and Western blotting were used to examine Bcl-2, Bax and caspase-3 protein levels in HepG2 cells treated with PE. RESULTS: PE inhibited the growth of HepG2 cells in a doseand timedependent manner. It did notaffect the cell cycle, but induced apoptosis. PE significantly decreased ΔΨm at 0.25, 0.5 and 1 mmol/L, respectively, suggesting that PE induces cell apoptosis by decreasing the mitochondrial transmembrane potential. The Bcl-2 expression level induced by different concentrations of PE was lower than that in control groups. However, the Bax expression level induced by PE was higher than that in the control group. Meanwhile, PE increased the caspase-3 expression in a doseand time-dependent manner. CONCLUSION: Exogenous PE induces apoptosis of human hepatoma HepG2 cells via the bcl-2/bax pathway.展开更多
AIM:To investigate the effect of α-mangostin on the growth and apoptosis induction of human colon cancer cells.METHODS:The three colorectal adenocarcinoma cell lines tested (COLO 205,MIP-101 and SW 620) were treated ...AIM:To investigate the effect of α-mangostin on the growth and apoptosis induction of human colon cancer cells.METHODS:The three colorectal adenocarcinoma cell lines tested (COLO 205,MIP-101 and SW 620) were treated with α-mangostin to determine the effect on cell proliferation by MTT assay,cell morphology,chromatin condensation,cell cycle analysis,DNA fragmentation,phosphatidylserine exposure and changing of mitochondrial membrane potential.The molecular mechanisms of α-mangostin mediated apoptosis were further investigated by Western blotting analysis including activation of caspase cascade,cytochrome c release,Bax,Bid,p53 and Bcl-2 modifying factor.RESULTS:The highest inhibitory effect of α-mangostin on cell proliferation of COLO 205,MIP-101 and SW 620 were 9.74 ± 0.85 μg/mL,11.35 ± 1.12 μg/mL and 19.6 ± 1.53 μg/mL,respectively.Further study showed that α-mangostin induced apoptotic cell death in COLO 205 cells as indicated by membrane blebbing,chromatin condensation,DNA fragmentation,cell cycle analysis,sub-G1 peak (P < 0.05) and phosphatidylserine exposure.The executioner caspase,caspase-3,the initiator caspase,caspase-8,and caspase-9 were expressed upon treatment with α-mangostin.Further studies of apoptotic proteins were determined by Western blotting analysis showing increased mitochondrial cytochrome c release,Bax,p53 and Bmf as well as reduced mitochondrial membrane potential (P < 0.05).In addition,up-regulation of tBid and Fas were evident upon treatment with α-mangostin (P < 0.01).CONCLUSION:α-Mangostin may be effective as an anti-cancer agent that induced apoptotic cell death in COLO 205 via a link between extrinsic and intrinsic pathways.展开更多
基金Supported by The National Natural Science Foundation of China (No. 30872481)the Scientific and Technological Planning Foundation of Shaanxi Province (No. 2006K09-G7-1)
文摘AIM: To investigate the signaling pathways implicated in phosphatidylethanolamine (PE)-induced apoptosis of human hepatoma HepG2 cells. METHODS: Inhibitory effects of PE on human hepatoma HepG2 cells were detected by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Cell cycle, apoptosis and mitochondrial transmembrane potential (ΔΨm) were analyzed by flow cytometry. Immunocytochemical assay and Western blotting were used to examine Bcl-2, Bax and caspase-3 protein levels in HepG2 cells treated with PE. RESULTS: PE inhibited the growth of HepG2 cells in a doseand timedependent manner. It did notaffect the cell cycle, but induced apoptosis. PE significantly decreased ΔΨm at 0.25, 0.5 and 1 mmol/L, respectively, suggesting that PE induces cell apoptosis by decreasing the mitochondrial transmembrane potential. The Bcl-2 expression level induced by different concentrations of PE was lower than that in control groups. However, the Bax expression level induced by PE was higher than that in the control group. Meanwhile, PE increased the caspase-3 expression in a doseand time-dependent manner. CONCLUSION: Exogenous PE induces apoptosis of human hepatoma HepG2 cells via the bcl-2/bax pathway.
基金Supported by The Thailand Research Fund,Grant No. RMU 4980043
文摘AIM:To investigate the effect of α-mangostin on the growth and apoptosis induction of human colon cancer cells.METHODS:The three colorectal adenocarcinoma cell lines tested (COLO 205,MIP-101 and SW 620) were treated with α-mangostin to determine the effect on cell proliferation by MTT assay,cell morphology,chromatin condensation,cell cycle analysis,DNA fragmentation,phosphatidylserine exposure and changing of mitochondrial membrane potential.The molecular mechanisms of α-mangostin mediated apoptosis were further investigated by Western blotting analysis including activation of caspase cascade,cytochrome c release,Bax,Bid,p53 and Bcl-2 modifying factor.RESULTS:The highest inhibitory effect of α-mangostin on cell proliferation of COLO 205,MIP-101 and SW 620 were 9.74 ± 0.85 μg/mL,11.35 ± 1.12 μg/mL and 19.6 ± 1.53 μg/mL,respectively.Further study showed that α-mangostin induced apoptotic cell death in COLO 205 cells as indicated by membrane blebbing,chromatin condensation,DNA fragmentation,cell cycle analysis,sub-G1 peak (P < 0.05) and phosphatidylserine exposure.The executioner caspase,caspase-3,the initiator caspase,caspase-8,and caspase-9 were expressed upon treatment with α-mangostin.Further studies of apoptotic proteins were determined by Western blotting analysis showing increased mitochondrial cytochrome c release,Bax,p53 and Bmf as well as reduced mitochondrial membrane potential (P < 0.05).In addition,up-regulation of tBid and Fas were evident upon treatment with α-mangostin (P < 0.01).CONCLUSION:α-Mangostin may be effective as an anti-cancer agent that induced apoptotic cell death in COLO 205 via a link between extrinsic and intrinsic pathways.
