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目的研究硒化壳聚糖增强ST1571对多药耐药白血病K562/ADM细胞敏感性的作用,并进一步探讨其耐药逆转机制。方法应用MTT法检测ST1571单独和联合硒化壳聚糖对K562/ADM细胞增殖的影响,计算逆转倍数;应用流式细胞法检测细胞凋亡;应用免疫印迹法检测核因子КB(NF-КB)蛋白的改变。结果单独应用1μmol·L-1ST1571作用12,24,36 h,对K562/ADM细胞增殖抑制率分别为(19.15±1.64)%、(24.35±2.37)%和(26.37±2.39)。1μmol·L-1ST1571联合25~400 mg·L-1硒化壳聚糖作用K562/ADM细胞,随着硒化壳聚糖浓度和作用时间的增加,对细胞增殖抑制率也相应增加,呈剂量时间效应关系。硒化壳聚糖能够对K562/ADM细胞耐ST1571产生一定的逆转作用,明显增强ST1571对K562/ADM细胞的诱导凋亡作用(P<0.05,P<0.01),下调NF-КB蛋白表达(P<0.01)。结论硒化壳聚糖能够增强K562/ADM细胞对ST1571的敏感性,其部分机制可能是通过诱导细胞凋亡,抑制细胞mdr-1基因表达,阻断细胞NF-КB信号通路来实现的。
Objective To study the effect of selenium chitosan on enhancing the sensitivity of ST1571 cells to multidrug-resistant leukemia K562 / ADM cells and to explore its mechanism of drug resistance reversal. Methods The effect of ST1571 alone or in combination with selenium chitosan on the proliferation of K562 / ADM cells was detected by MTT assay, and the fold of reversal was calculated. Flow cytometry was used to detect the apoptosis. The expression of nuclear factor КB (NF-КB) Protein changes. Results The inhibition rates of K562 / ADM cells treated with 1μmol·L-1ST1571 alone for 12, 24, 36 h were (19.15 ± 1.64)%, (24.35 ± 2.37)% and (26.37 ± 2.39), respectively. Chitosan inhibited the proliferation of K562 / ADM cells treated with 1 μmol·L-1ST1571 and 25-400 mg · L-1 selenium-enriched chitosan. With the increase of selenium concentration and time, Time effect relationship. Selenized chitosan could reverse the effect of ST1571 in K562 / ADM cells and induce apoptosis of K562 / ADM cells (P <0.05, P <0.01), and down-regulate the expression of NF-КB protein <0.01). Conclusion Selenized chitosan can enhance the sensitivity of K562 / ADM cells to ST1571. Part of the mechanism may be through inducing apoptosis, inhibiting the expression of mdr-1 gene and blocking the NF-КB signaling pathway in K562 / ADM cells.