Kaĭgorodova E V, Riazantseva N V, Novitskiĭ V V, Moroshkina A N, Belkina M V, Iakushina V D
Vestn Ross Akad Med Nauk. 2011(8):3-6.
rTNFalpha-induced programmed death of Jurkat tumor cells cultured with 17-AAG, a selective inhibitor of heat shock protein (Hsp90), was studied by fluorescent microscopy with the use of FITC-labeled annexin V and propidium iodide. Caspase-3 and -8 activities were determined by spectrophotometry using a caspase- 3 and -8 colorimetric assay kit. It was shown that inhibition of Hsp90 leads to activation of Jurkat cell apoptosis while Hsp90 itself suppresses this process. 17-AAG enhances rTNFa-induced apoptosis of tumor cells.
利用异硫氰酸荧光素（FITC）标记的膜联蛋白V和碘化丙啶，通过荧光显微镜研究了重组人肿瘤坏死因子α（rTNFα）诱导的、与热休克蛋白（Hsp90）选择性抑制剂17-烯丙基氨基-17-去甲氧基格尔德霉素（17-AAG）一起培养的Jurkat肿瘤细胞的程序性死亡。使用半胱天冬酶-3和-8比色检测试剂盒，通过分光光度法测定半胱天冬酶-3和-8的活性。结果表明，抑制Hsp90会导致Jurkat细胞凋亡的激活，而Hsp90本身会抑制这一过程。17-AAG增强了rTNFα诱导的肿瘤细胞凋亡。
