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目的研究三氧化二砷(arsenic trioxide,ATO)前后人多发性骨髓瘤ARH-77对NK细胞杀伤细胞敏感性的变化,并初步探讨其机制。方法分别应用CCK-8法和台盼蓝染色法测算ATO对ARH-77细胞株的50%抑制量(IC50)和细胞活性;乳酸脱氢酶释放法检测ATO作用前后ARH-77细胞对NK细胞的杀伤敏感性。流式细胞仪检测ARH-77细胞表面NKG2D配体(MICA/B、ULBP1、ULBP2、ULBP3)和HLA-Ⅰ类分子表达以及ATO作用前后的细胞周期变化。结果ATO对ARH-77细胞的IC50为5.0μmol/L。NK细胞杀伤ATO作用前后ARH-77细胞的活性有显著差异(P<0.05)。ATO作用后,ARH-77细胞发生G1/S期阻滞,同时其表面MICA/B、ULBP1、ULBP3表达显著升高,二者之间差异有统计学意义(P<0.05)。ULBP2和HLA-Ⅰ类分子无明显变化(P>0.05)。结论ATO能提高ARH-77细胞NKG2D配体(MICA/B、ULBP1、ULBP3)表达;从而使其对NK细胞的杀伤敏感性增强。
Objective To study the changes of killer cell sensitivity of human multiple myeloma ARH-77 cells before and after arsenic trioxide (ATO), and to explore its mechanism. Methods The IC50 and cell viability of ARH-77 cell line were measured by CCK-8 assay and trypan blue staining respectively. The effect of ATO on the proliferation of NK cells Kill sensitivity. Flow cytometry was used to detect the expression of NKG2D ligand (MICA / B, ULBP1, ULBP2, ULBP3) and HLA class I molecules on ARH-77 cells and the cell cycle changes before and after ATO treatment. Results The IC50 of ATO on ARH-77 cells was 5.0 μmol / L. The activity of ARH-77 cells before and after NK cell killing ATO was significantly different (P <0.05). After ATO treatment, G1 / S phase arrest was observed in ARH-77 cells, while the expression of MICA / B, ULBP1 and ULBP3 on the surface of ARH-77 cells was significantly increased. The difference was statistically significant (P <0.05). ULBP2 and HLA-Ⅰ molecules had no significant changes (P> 0.05). Conclusion ATO can increase the expression of NKG2D ligands (MICA / B, ULBP1, ULBP3) in ARH-77 cells and enhance the sensitivity to NK cells.