中文摘要：

在现在的学习，我们在 Jurkat T 白血病房间调查了在 proteasome 禁止者 carfilzomib (CFZ ) 和 histone deacetylaseinhibitor vorinostat 之间的相互作用。到 CFZ 与的最低限度地致命的集中的细胞的 Coexposure 很， vorinostat 的 lowconcentration 导致了 synergistic antiproliferative 效果并且在 Jurkat T-leukemiacells 提高了 apoptosis ，与严厉地增加的反应的氧种( ROS )伴随了，在 mitochondrial membranepotential ( MMP )的惹人注目的减少，细胞色素 c 的增加的版本， caspase-9 和-3,和 PARP.The 的劈开的提高的激活联合了 Jurkat 细胞的处理与 ROS 预先对待而且， NAC 也在 apoptotic 房间导致了显著减小，显示为由联合处理的 increasedROS 产生的一个关键角色。另外，联合了逮捕的处理在 G ₂-M 的房间周期阶段。这些结果暗示 CFZ 在 Jurkat T 白血病房间与 vorinostat synergistically 交往了，哪个有 vorinostat 的 carfilzomib 的联合可以在对待 T 房间代表新奇策略的 raisedthe 可能性白血病。

英文摘要：

In the present study, we investigated the interactions between proteasome inhibitor carfllzomib （CFZ） and histone deacety lase inhibitor vorinostat in Jurkat Tleukemia ceils. Coexposure of cells to minimally lethal concentrations of CFZ with very low concentration of vorinostat resulted in synergistic antiproliferative effects and enhanced apoptosis in Jurkat Tleukemia cells, accompanied with the sharply increased reactive oxygen species （ROS）, the striking de crease in the mitochondrial membrane potential （MMP）, the increased release of cytochrome c, the enhanced activation of caspase9 and 3, and the cleavage of PARP. The com bined treatment of Jurkat cells pretreated with ROS sca vengers Nacetylcysteine （NAC） significantly blocked the loss of mitochondrial membrane potential, suggesting that ROS generation was a former event of the loss of mitochon drial membrane potential. Furthermore, NAC also resulted in a marked reduction in apoptotic cells, indicating a critical role for increased ROS generation by combined treatment. In addition, combined treatment arrested the cell cycle in G2M phase. These results imply that CFZ interacted syner gistically with vorinostat in Jurkat Tleukemia cells, which raised the possibility that the combination of carfflzomib with vorinostat may represent a novel strategy in treating Tcell Leukemia.