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目的:探讨热休克蛋白90(heat shock protain 90,HSP90)分子伴侣复合物阻止剂17-丙烯胺基-17去甲氧基格尔德霉素(17-allyl-amide-17-demethoxgeldanamycin,17-AAG),对热诱导的骨肉瘤SOSP-9607细胞杀伤作用的影响。方法:采用干细胞集落形成实验、流式细胞术(flow cytometry,FCM)和吖啶橙荧光染色等方法观察比较单纯热疗组与热疗联合17-AAG治疗组对骨肉瘤SOSP-9607细胞活力、凋亡率及形态学影响。结果:干细胞集落形成实验显示,热疗联合17-AAG治疗组较单独热疗对骨肉瘤SOSP-9607细胞的杀伤效应明显增强,P=0.036;Annexin V-FITC染色流式细胞术结果显示,热疗联合17-AAG治疗组所致凋亡率(52.2%)大于单纯热疗组(17.5%);用吖啶橙荧光染色法观察到热疗联合17-AAG治疗组明显见骨肉瘤SOSP-9607细胞固缩着色不均而且较深,细胞核浓缩、裂解等凋亡特征。结论:HSP90分子伴侣复合物阻止剂17-AAG能增强热诱导的骨肉瘤SOSP-9607细胞的杀伤作用。
Objective: To investigate the effect of 17-allyl-amide-17-demethoxgeldanamycin (17-allyl-17-demethoxgeldanamycin), a heat shock protein 90 (HSP90) molecular chaperone inhibitor, AAG) on the cytotoxicity of heat-induced osteosarcoma SOSP-9607 cells. Methods: SOSP-9607 cells were treated with 17-AAG combined with hyperthermia and 17-AAG group respectively by flow cytometry (FCM) and acridine orange staining. Apoptosis and morphological effects. Results: The results of stem cell colony formation assay showed that the killing effect of hyperthermia combined with 17-AAG treatment group on osteosarcoma SOSP-9607 cells was significantly enhanced compared with that of hyperthermia alone group (P = 0.036). The results of flow cytometry with Annexin V-FITC showed that heat- Apoptosis rate (52.2%) in combination with 17-AAG treatment group was greater than that in simple hyperthermia group (17.5%); acridine orange fluorescence staining was observed in hyperthermia combined with 17-AAG treatment group was significantly osteosarcoma SOSP-9607 Cell shrinkage is uneven and darker, nuclear condensation, lysis and other apoptotic features. Conclusion: HSP90 chaperone complex inhibitor 17-AAG can enhance the killing effect of heat-induced osteosarcoma SOSP-9607 cells.