首页> 中文期刊> 《复旦学报(医学版)》 >凋亡调节蛋白的表达与K562/VCR多药耐药性的关系

凋亡调节蛋白的表达与K562/VCR多药耐药性的关系

         

摘要

目的 探讨K562/VCR细胞中凋亡调节蛋白表达的变化与其多药耐药性(MDR)的关系。方法 通过免疫细胞化学法和免疫印迹法(western blot)对凋亡调节蛋白Bcl-2、Bcl-XL、Bax、Bak在多药耐药细胞K562/VCR和药物敏感细胞K562中的表达进行分析。结果 抗凋亡调节蛋白Bcl-2、Bcl-XL在K562/VCR细胞中的表达阳性率分别为(40.0±8.0)%和(60.0±10.0)%,在K562细胞中为(1.0±0 3)%和(20.0±40)%,阳性率差异均具有显著性(n=3,P<0.05)。促凋亡调节蛋白Bax在以上两种细胞中的表达程度无明显区别促凋亡调节蛋白Bak在两种细胞中均不表达或表达程度极低。结论抗凋亡调节蛋白(Bcl-2、Bcl-XL)在K562/VCR细胞MDR发生中可能发挥重要作用,而促凋亡调节蛋白Bax、Bak可能不起主要作用。%Purpose To explore the Relationship between expression of apoptosis-modulating proteins amdmultidrug resistance in K562/VCR cells. Methods Irnmunocytochemical methol and western blot wereused to analyze the expression of apoptosis-modulating proteins (Bcl - 2, Bcl-XL, Bax, Bak ) in multidrugresistant cell line K562/VCR and drugsensitive cell line K562. Results The positive cell rates ofapoptosis-suppressing protein Bcl-2 and Bcl-XL in K562/VCR were (40.0 ± 8.0) % and (60.0 ± 10.0) % .While the rates in K562 were (1.0 ± 0.3) % and (20.0 ± 4.0) %. There was significant difference in thepositive cell rates of Bcl - 2 and Bcl - XL between K562/VCR and K562 ( n = 3, P < 0.05 ). It was alsofound there was no significant difference in expression of Bax between K562/VCR and K562. Furthemore,Bak was not expressed in both K562/VCR and K562 or the expression was very low. Conclusions Wesuggest that Bcl-2 and Bcl-XL play important roles in multidrug resistance in K562/VCR, while Bax and Bakmight not be important.

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