白介素-17对骨髓瘤细胞增殖和凋亡的影响

Effect of interleukin-17 on proliferation and apoptosis of myeloma cells

目的探讨白介素-17(interleukin-17,IL-17)对骨髓瘤细胞株RPMI8226增殖和凋亡的影响及骨髓瘤细胞株IL-17R的表达。方法体外培养RPMI8226细胞,取对数生长期的细胞,分别加入浓度为25、50、100、200、500 ng/ml的rh IL-17(另设不加rh IL-17的对照组),共同培养72 h后,采用MTT法检测IL-17对RPMI8226细胞增殖的影响;TUNEL法检测IL-17对RPMI8226细胞凋亡的影响。将BALB/c雌性小鼠随机分为试验组和对照组,分别经腹部皮下注射含100 ng/ml IL-17和不含IL-17的RPMI8226细胞(5×106个),观察肿瘤生长情况。应用流式细胞术检测RPMI8226细胞IL-17R的表达。结果不同浓度的IL-17与对照组相比,均可促进RPMI8226细胞的增殖(P﹤0.05),抑制细胞凋亡(P﹤0.05)。经IL-17处理的RPMI8226细胞荷瘤小鼠与对照组相比,成瘤时间缩短(P﹤0.05),肿瘤体积增大(P﹤0.05)。RPMI8226细胞显著表达IL-17R。结论 IL-17在体内外均可促进RPMI8226细胞增殖,抑制其凋亡;RPMI8226细胞显著表达IL-17R。

Objective To investigate the effect of interleukin（IL）- 17 on proliferation apoptosis of myeloma cell RPMI8226 strain as well as the expression of IL-17 receptor（IL-17R） in RPMI8226 cells. Methods RPMI8226 cells were cultured in vitro, of which those in logarithmic growth phase were treated with recombinant human IL-17（rh IL-17）at concentrations of 25, 50, 100, 200 and 500 ng / ml for 72 h, using those untreated as control. The effect of IL-17 on proliferation of RPMI8226 cells was evaluated by MTT assay, while that on apoptosis of the cells by TUNEL assay. Female BALB / c mice were divided into test and control groups, and injected s. c. with 5 × 10^6RPMI8226 cells treated with100 ng / ml IL-17 and untreated cells respectively, and observed for the tumor growth. The expression of IL-17 R in RPMI8226 cells was determined by flow cytometry. Results The IL-17 at various concentrations promoted the proliferation and inhibited the apoptosis of RPMI8226 cells（each P〈0. 05） as compared with that in control group. The time duration for tumor formation in the mice in test group was shortened as compared with that in control group（P〈0. 05）,while the tumor size increased（P〈0.05）. IL-17 R was expressed significantly in RPMI8226 cells. Conclusion IL-17 promoted the proliferation and inhibited the apoptosis of RPMI8226 cells in vitro and in vivo, and the cells were suitable for the expression of IL-17 R.