目的:探讨姜黄素(curcumin,Cur)对人多发性骨髓瘤ARH-77细胞外源性凋亡通路的影响。方法:ARH-77细胞经6.25、12.5、25、50、100、200μmol/L Cur处理12、24、48 h,MTT法检测Cur对ARH-77细胞增殖的抑制作用,Hoechst 33258染色法观察Cur处理24 h后ARH-77细胞凋亡的形态学改变,流式细胞术检测ARH-77细胞周期和Fas/FasL、TRAIL/TRAIL-R的表达,分光光度法检测ARH-77细胞caspase-8的活性。结果:Cur对ARH-77细胞的增殖有时间和剂量依赖的抑制作用。25μmol/L Cur处理ARH-77细胞可观察到凋亡小体,Cur阻滞细胞周期于G0/G1期,并且有凋亡峰。其促凋亡作用呈浓度依赖性,6.25、12.5、25μmol/L Cur作用24 h后,ARH-77细胞凋亡率均显著高于对照组[(10.35±0.35)%、(14.35±1.34)%、(36.65±1.06)%vs(3.83±0.32)%,F=500.432,P=0.000];实验组细胞内caspase 8的活化程度均显著高于对照组[(0.223±0.018)、(0.263±0.019)、(0.240±0.035)vs(0.154±0.007);F=9.059,P=20.03]。12.5μmol/L Cur作用24 h后,ARH-77细胞表面Fas[(99.05±0.49)%vs(92.10±0.70)%,t=15.404,P=0.000]、FasL[(9.05±0.78)%vs(1.73±1.19)%,t=9.487,P=0.008]、TRAIL[(1.35±0.07)%vs(0.55±0.07)%,t=-11.317,P=0.008]、DR4、DcR1和DcR2的表达均显著升高,DR5表达显著降低[(0.95±0.07)%vs(7.70±0.29)%,t=32.742,P=0.001];进一步提升Cur浓度至25μmol/L,却降低了DcR1[(4.35±1.20)%vs(14.25±0.21)%;t=5.692,P=0.008]及DcR2[(0.75±0.21)%vs(1.65±0.71)%;t=11.470,P=0.03]的表达。结论:Cur能明显抑制人多发性骨髓瘤ARH-77细胞的增殖,其机制可能与激活外源性凋亡通路从而诱导细胞凋亡有关。 Objective: To investigate the effect of curcumin (Cur) on the extrinsic apoptotic pathway of human multiple myeloma ARH-77 cells. Methods: ARH-77 cells were treated with 6, 25, 25, 25, 50, 100 and 200 μmol / L Cur for 12, 24 and 48 h respectively. The inhibitory effect of Cur on the proliferation of ARH-77 cells was detected by MTT assay. Curcumin treatment was performed by Hoechst 33258 staining The morphological changes of ARH-77 cells were observed after 24 h. The expression of Fas / FasL and TRAIL / TRAIL-R were detected by flow cytometry. The activity of caspase-8 in ARH-77 cells was detected by spectrophotometry . Results: Cur inhibited the proliferation of ARH-77 cells in a time and dose-dependent manner. Apoptotic bodies were observed in ARH-77 cells treated with 25μmol / L Cur, while Cur inhibited the cell cycle in G0 / G1 phase with apoptotic peak. The apoptotic rate of ARH-77 cells was significantly higher than that of the control group [(10.35 ± 0.35)%, (14.35 ± 1.34)%, P <0.05] (36.65 ± 1.06)% vs (3.83 ± 0.32)%, F = 500.432, P = 0.000]. The activation of caspase 8 in the experimental group was significantly higher than that in the control group [(0.223 ± 0.018), (0.263 ± 0.019, ), (0.240 ± 0.035) vs (0.154 ± 0.007); F = 9.059, P = 20.03]. Fas (99.05 ± 0.49)% vs (92.10 ± 0.70)%, t = 15.404, P = 0.000], FasL [(9.05 ± 0.78)% vs 1.73 ± 1.19%, t = 9.487, P = 0.008], TRAIL [(1.35 ± 0.07)% vs (0.55 ± 0.07)%, t = -11.317, P = 0.008]. The expression of DR4, DcR1 and DcR2 were all significantly (0.95 ± 0.07)% vs (7.70 ± 0.29)%, t = 32.742, P = 0.001]. When Cur concentration was further increased to 25 μmol / L, DcR1 [(4.35 ± 1.20) % vs (14.25 ± 0.21)%; t = 5.692, P = 0.008] and DcR2 [(0.75 ± 0.21)% vs (1.65 ± 0.71)%; t = 11.470, P = 0.03]. CONCLUSION: Cur can significantly inhibit the proliferation of human multiple myeloma ARH-77 cells. The mechanism may be related to the activation of exogenous apoptosis pathway and the induction of apoptosis.