本文選題：硼替佐米 + K細(xì)胞　； 參考：《中國實驗血液學(xué)雜志》2013年04期

【摘要】：本研究旨在探討蛋白酶體抑制劑硼替佐米(bortezomib)對K562細(xì)胞的增殖、凋亡及SHIP基因表達的影響。將不同濃度的硼替佐米作用于K562細(xì)胞,采用MTT法測定細(xì)胞增殖活性,用流式細(xì)胞術(shù)檢測細(xì)胞凋亡,RT-PCR方法檢測SHIP mRNA表達。結(jié)果表明,硼替佐米10、20、50和100 nmol/L作用于K562細(xì)胞24 h,細(xì)胞增殖抑制率分別為(5.76±1.47)%、(10.55±1.59)%、(17.14±2.05)%和(27.69±3.57)%,空白對照組為(1.30±0.10)%;20nmol/L硼替佐米作用于K562細(xì)胞24、48、72 h,細(xì)胞增殖抑制率分別為(10.55±1.59)%、(16.33±2.53)%、(19.78±1.56)%,24 h組與48 h組比較,差異具有統(tǒng)計學(xué)意義(P0.05),10、20、50、100 nmol/L硼替佐米作用于K562細(xì)胞24h,Annexin V-FITC/PI雙標(biāo)法顯示其凋亡率分別為(12.7±0.6)%、(26.9±0.9)%、(32.6±1.2)%、(72.5±1.5)%,均高于對照組(1.0±0.5)%(P0.05)。RT-PCR法檢測結(jié)果顯示應(yīng)用硼替佐米作用后SHIP mRNA表達上調(diào)明顯,與空白對照組比較差異有統(tǒng)計學(xué)意義。結(jié)論:硼替佐米呈時間、濃度依賴性抑制K562細(xì)胞增殖,并能通過上調(diào)SHIP基因的表達誘導(dǎo)細(xì)胞凋亡。
[Abstract]:The aim of this study was to investigate the effects of bortezomibb, a proteasome inhibitor, on the proliferation, apoptosis and SHIP gene expression of K562 cells. The proliferation activity of K562 cells was determined by MTT assay, and the expression of SHIP mRNA was detected by flow cytometry and reverse transcription-polymerase chain reaction (RT-PCR). The results showed that the inhibition rates of proliferation of K562 cells were 5.76 鹵1.47% and 17.14 鹵2.05% and 27.69 鹵3.57%, respectively, when bortezomil 1020 and 100 nmol/L were applied to K562 cells for 24 h and 100 nmol/L, respectively, while those in the blank control group were 1.30 鹵0.1020 nmol / L borizomil for 24448 hours, and the inhibition rates of cell proliferation were 10.55 鹵1.59m and 16.33 鹵2.53, 19.78 鹵1.56 and 19.78 鹵1.56g / h, respectively. The difference was statistically significant (P 0.05, P 0. 05, P 0. 05, 10, 20, 50, 100 nmol/L bortezomil) treated K562 cells for 24 h, Annexin V-FITC/PI double labeling method showed that the apoptotic rate was 26. 9 鹵0. 9 鹵0. 9%. The expression of SHIP mRNA in K562 cells was significantly higher than that in the control group (1. 0 鹵1. 5 鹵1. 5 鹵1. 5 鹵1. 5). The results showed that the expression of SHIP mRNA was up-regulated after treatment with bortezomil. Compared with the blank control group, the difference was statistically significant. Conclusion: bortezomil can inhibit the proliferation of K562 cells in a dose-dependent manner and induce apoptosis by up-regulating the expression of SHIP gene.
【作者單位】： 保定市第一醫(yī)院血液科;
【分類號】：R363

【參考文獻】

相關(guān)期刊論文 前4條

1 楊琳;羅建民;劉小軍;溫樹鵬;杜行嚴(yán);姚麗;楊敬慈;;SHIP基因誘導(dǎo)白血病細(xì)胞株K562凋亡及其機制[J];生理學(xué)報;2009年02期

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本文編號：1819617