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研究G¨o6 976是否能去除As2 O3引起的G2 M周期阻滞 ,增加慢性髓系白血病 (CML)细胞株 (K5 6 2细胞 )对As2 O3的敏感性。K5 6 2细胞经不同浓度的G¨o6 976及和As2 O3(5 μmol L)作用后 ,流式细胞术检测细胞周期 ,台盼蓝排斥试验检测细胞活力 ,四唑盐 (MTT)比色试验分析细胞的生长增殖。结果表明 ,流式细胞术细胞周期检测发现K5 6 2细胞经As2 O3作用 2 4小时和 4 8小时后 ,G2 M期细胞比例分别为 (38.0 2± 7.70 ) %和 (32 .5 8± 7.4 3) % ,未出现明显凋亡 ;5 0nmol LG¨o6 976与As2 O3联合作用后 ,G2 M期细胞分别减少至 (2 3.2 4± 2 .93) %和 (16 .18±1.6 0 ) % ,subG1 期细胞分别增加至 (11.82± 2 .31) %和 (2 7.80± 2 .89) % ;且其变化随G¨o6 976浓度及作用时间而增加。同时台盼蓝排斥试验及MTT试验观察到G¨o6 976与As2 O3联合作用能明显降低细胞活力、抑制其生长 ,但G¨o6 976本身无明显作用。结论 :G¨o6 976可能通过去除G2 M期阻滞 ,有效增强了K5 6 2细胞对As2 O3化疗的敏感性。
To investigate whether G¨ό6 976 can eliminate G2 M cycle arrest induced by As2 O3 and increase the sensitivity of As2O3 to CML cell line (K5 6 2 cells). K562 cells were treated with different doses of G¨¨0 6 976 and As 2 O 3 (5 μmol L), cell cycle was detected by flow cytometry, trypan blue exclusion assay was used to detect cell viability, MTT colorimetric assay Analysis of cell growth and proliferation. The results of flow cytometry showed that the percentage of cells in G2 M phase was (38.0 2 ± 7.70)% and (32.58 ± 7.4)% respectively at 24 and 48 hours after treated with As 2 O 3 3)%, no obvious apoptosis occurred. After treated with 500 nmol LG¨O6 976 and As2 O3, cells in G2 M phase were reduced to (2 3.2 4 ± 2.93)% and (16.18 ± 1.6 0)%, respectively , while the number of subG1 phase cells increased to (11.82 ± 2.31)% and (2. 7.80 ± 2.89)%, respectively, and the changes increased with the concentration and duration of action. At the same time, the trypan blue exclusion test and MTT assay showed that the combined effect of G¨¨O6 976 and As2 O3 could significantly reduce the cell viability and inhibit the growth of G¨o6 976 itself. CONCLUSION: G¨O6 976 may enhance the sensitivity of K562 cells to As2O3 treatment by removing G2 M arrest.