出 处:《Acta Pharmacologica Sinica》2008年第10期1233-1239,共7页中国药理学报(英文版)
基 金:Project supported by National Natural Science Foundation of China (No 30300426). Author contribution Xiao-yong LEI designed research; Shu-qiong YAO, Ze-xiang HUANG, Li-juan LIU and Bing-yang ZHU performed research; Miao ZHONG, Sheng-song TANG and Duan-fang LIAO contributed new analytical tools and reagents; Xiao-yong LEI and Xu-yu ZU analyzed data; Shu-qiong YAO and Xiao-yong LEI wrote the paper.
摘 要:Aim: To investigate the effect of diallyl disulfide (DADS), a component of garlic, on apoptosis in human mammary cancer cell line (MCF-7) and its mechanisms. Methods: Cytotoxicity was analyzed by 3-(4,5-dimethylthiazol-2-yl)-2,5- diphenyltetrazolium bromide assays. Morphology of apoptotic cells was detected by acridine orange and ethidium bromide staining. Apoptotic cells stained with propidium iodide were examined using flow cytometry. Protein levels were detected by Western blot analysis. Results: DADS inhibited the proliferation of MCF-7 cells and induced the apoptotic ratio to increase rapidly. Cleavage of the caspase-3 and caspase-3 substrate poly(ADP-ribose) polymerase was observed in MCF-7 cells after 24 h of treatment with DADS. When the MCF-7 cells were treated with 200 μmol·L^-1 DADS, the stress-activated protein kinase extracellular signal-regulated kinase (ERK), a mitogen-activated protein kinase, was inhibited after 6 h; c-Jun N-terminal kinase (JNK), that is stress-activated protein kinase (SAPK), and p38 mitogen-activated protein kinase were activated after 6 h. Conclusion: These results suggest that DADS both inhibits the proliferation of MCF-7 cells and induces apoptosis of MCF-7 cells. The mechanisms may include the inhibition of ERK and the activation of the SAPK/JNK and p38 pathways.Aim: To investigate the effect of diallyl disulfide (DADS), a component of garlic, on apoptosis in human mammary cancer cell line (MCF-7) and its mechanisms. Methods: Cytotoxicity was analyzed by 3-(4,5-dimethylthiazol-2-yl)-2,5- diphenyltetrazolium bromide assays. Morphology of apoptotic cells was detected by acridine orange and ethidium bromide staining. Apoptotic cells stained with propidium iodide were examined using flow cytometry. Protein levels were detected by Western blot analysis. Results: DADS inhibited the proliferation of MCF-7 cells and induced the apoptotic ratio to increase rapidly. Cleavage of the caspase-3 and caspase-3 substrate poly(ADP-ribose) polymerase was observed in MCF-7 cells after 24 h of treatment with DADS. When the MCF-7 cells were treated with 200 μmol·L^-1 DADS, the stress-activated protein kinase extracellular signal-regulated kinase (ERK), a mitogen-activated protein kinase, was inhibited after 6 h; c-Jun N-terminal kinase (JNK), that is stress-activated protein kinase (SAPK), and p38 mitogen-activated protein kinase were activated after 6 h. Conclusion: These results suggest that DADS both inhibits the proliferation of MCF-7 cells and induces apoptosis of MCF-7 cells. The mechanisms may include the inhibition of ERK and the activation of the SAPK/JNK and p38 pathways.
关 键 词:diallyl disulfide human mammary cancer cells (MCF-7) APOPTOSIS signaling pathway mitogen-activated protein kinase extracellular signal-regulated kinase (ERK) p38 mitogen-activated protein kinase (MAPK) c-Jun Nterminal kinase (JNK)
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