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作 者:陈敏[1,2] 张珍珍[1] 丁晔[3] 张奕华[3] 季晖[1]
机构地区:[1]中国药科大学药理学教研室,南京210009 [2]连云港中医药高等职业技术学校,连云港222006 [3]中国药科大学新药研究中心,南京210009
出 处:《中国药科大学学报》2011年第3期247-250,共4页Journal of China Pharmaceutical University
摘 要:对一氧化氮(NO)供体型齐墩果烷衍生物(SO-10)对肝癌的抑制作用进行了研究。检测了NO在其诱导肝癌细胞凋亡中的作用。MTT法检测显示SO-10能显著抑制肝癌细胞株(HepG2、BEL-7402和SMMC-7721)的增殖,SO-10作用48 h后的IC50分别为HepG2(1.19±0.12μmol/L)、BEL-7402(1.98±0.85μmol/L)和SMMC-7721(5.92±0.58μmol/L);流式细胞仪检测显示0.5-2μmol/L的SO-10均诱导肝癌细胞株HepG2凋亡,细胞凋亡率随浓度增加而上升;G riess法显示SO-10作用后HepG2内的NO水平随着药物作用时间的延长而增加,用NO清除剂预处理后,随着NO浓度的降低,SO-10对HepG2细胞增殖的抑制作用也相应降低。提示SO-10对肝癌细胞有抗增殖作用和诱导凋亡作用,可能与SO-10在肝癌细胞中释放NO有关。To investigate the inhibition effects of NO-donating oleanane derivative(SO-10) on human hepatoma cell lines and the antitumor activities of NO,MTT assay was used to analyze human hepatoma cells(HepG2,BEL-7402 and SMMC-7721) proliferation.SO-10 strongly inhibited human hepatoma cell proliferation and their IC50 values were 1.19±0.12 μmol/L for HepG2,1.98±0.85 μmol/L for BEL-7402 and 5.92±0.58 μmol/L for SMMC-7721 after 48 h.Apoptosis of HepG2 cells induced by SO-10 was detected by flow cytometry(FCM),showing that SO-10 dramatically triggered apoptosis in HepG2 cells in a dose-dependent manner.The amount of NO produced by SO-10 were increased from 30 min to 6 h examined by the Griess assay.Furthermore,pre-treatment with different concentrations of hemoglobin notably reduced the concentrations of NO and inhibited the cytotoxicity of SO-10 against HepG2 cells.SO-10 showed remarkable effects of inhibiting cell proliferation and inducing apoptosis of human hepatoma cell lines.The significantly high concentrations of NO produced by SO-10 might contribute to its cytotoxicity against HepG2 cells.
关 键 词:一氧化氮供体型齐墩果烷衍生物 肝癌 细胞增殖 凋亡
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