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目的探讨普通胰岛素有无化疗增敏的作用及诱导细胞凋亡的原理。方法 2007年10月至2008年6月在华中科技大学同济医学院附属协和医院对Ishikawa,Hec-1A细胞经胰岛素和脂质体紫杉醇处理后,以3-(4,5)-双甲基-2-噻唑-(2,5)-二本基溴四氮唑蓝(MTT)法检测细胞的增殖情况;以流式细胞仪检测细胞凋亡。结果胰岛素联合脂质体紫杉醇合用72h时抑制率高达63.2%和50.2%,与脂质体紫杉醇单独作用相比差异有统计学意义(P<0.01)。两药合用时抑制率达到最高峰。结论体外脂质体紫杉醇可抑制Ishikawa和Hec-1A细胞增殖并诱导其发生凋亡,且与胰岛素联合应用时抑制作用明显增加。
Objective To investigate the effect of general insulin on chemosensitivity and the principle of inducing apoptosis. Methods From October 2007 to June 2008, Ishikawa and Hec-1A cells were treated with insulin and liposomal paclitaxel at the Third Affiliated Hospital of Tongji Medical College, Huazhong University of Science and Technology. The 3- (4,5) -dimethyl- The proliferation of cells was detected by MTT assay and apoptosis was detected by flow cytometry (FCM) with 2-thiazolyl- (2,5) -dibenzothiazolyl tetrazolium bromide (MTT). Results The inhibitory rates of insulin combined with liposomal paclitaxel at 72h were as high as 63.2% and 50.2%, respectively, which were significantly different from those of liposomal paclitaxel alone (P <0.01). The two drugs combined inhibition rate reached its peak. Conclusions Paclitaxel can inhibit the proliferation and induce the apoptosis of Ishikawa and Hec-1A cells in vitro, and its inhibitory effect is obviously increased when combined with insulin.