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- W3145291489 abstract "瞄准：在人的 HepG2 房间在房间增长和 apoptosis 上调查腺苷的效果。方法：HepG2 房间为 12-48 h 面对腺苷(0.1-5 mmol/L ) 被孵化，并且房间增长上的腺苷的效果被使用 3-(4,5-dimethyl-2-yl ) 评估 -2,5-diphenyl-2H-tetrazolium 溴化物(MTT ) 试金。Hoechst 33342 荧光灯的染色， dUTP 荧光黄异硫氰酸盐(FITC ) 荧光和流动 cytometric 分析技术被用来观察房间 apoptosis。腺苷受体(A1， A2a， A3 和非特定的受体) 的效果对手(8-cpt， DMPX， MRS1191，和茶硷) 和导致腺苷的房间 apoptosis 上的一个腺苷 transporter 蛋白质禁止者(dipyridamole ) 被观察。Mitochondrial 膜电位用 DePsipher 被分析荧光灯的染色，并且 caspase 活动用一个 Fluorometric 试金工具包和荧光被检测微板读者。结果：腺苷显著地在一个剂量依赖者和时间依赖者举止减少了房间生存能力。腺苷的细胞毒性与房间 apoptosis 的正式就职有关。四个腺苷受体对手没在房间 apoptosis 上有效果。然而， dipyridamole 显著地从 27.3% ～ 7.1% 减少了导致腺苷的 apoptotic 房间的百分比(P<0.05 ) 。在 48 h 术后疗法， 3 mmol/L 腺苷增加了 caspase-3 活动 3.5 褶层；dipyridamole 显著地减少了 caspase-3 活动 1.6 褶层，和减少的 apoptotic 房间数。当 HepG2 房间与 3 mmol/L 腺苷被对待时， mitochondrial 膜电位和 caspase-8 或 -9 的活动仍然保持未改变。结论：我们的结果建议在 HepG2 房间的导致腺苷的 apoptosis 与细胞内部的事件而非房间表面有关受体，和那 caspase-3 串联激活被要求，它没经由一条 mitochondrial 小径被调停。" @default.
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- W3145291489 date "2006-01-01" @default.
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- W3145291489 title "Molecular mechanisms of adenosine-induced apoptosis in human HepG2 cells" @default.
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