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目的研究姜黄素在人微血管内皮细胞增殖、迁移、成管以及凋亡的作用，并初步探讨其机制。方法将姜黄素分为0、20、40及80μmol/L四个实验组，分别用MTS 法、划痕实验、成管实验以及Hoechst 33258与TUNEL双重荧光检测姜黄素对人微血管内皮细胞增殖细胞增殖、迁移、成管以及凋亡的影响。结果 MTS结果显示：从姜黄素与HMVEC-Ls共同培养的第1d开始，(20-80)μmol/L三个浓度组均可抑制HMVEC-Ls增殖，与对照组(0μg/mL)相比差异有显著性(p<0.05)，尤以80μmol/L组抑制HMVEC-Ls增殖能力最显著(p<0.05)。划痕实验结果显示：(0-80)μmol/L四个姜黄素浓度组HMVEC-Ls迁移率分别为(92.33±5.01)%、(82.50±5.09)%、(63.00±5.73)%及(41.00±4.15)%，各实验组HMVEC-Ls迁移率差异有显著性(P<0.05)，其中尤以80μmol/L组HMVEC-Ls迁移率最低。成管实验。结果(0-80)μmol/L四个姜黄素浓度组HMVEC-Ls成管长度分别为(2.76±0.14)、(1.76±0.09)、(0.90±0.16)、(0.34±0.07)mm/视野，各实验组HMVEC-Ls成管长度差异有显著性(P<0.05)，其中尤以80μmol/L组HMVEC-Ls成管长度最小。Hoechst33258与TUNEL双重荧光染色。结果在姜黄素与HMVEC-Ls共同培养过程中HMVEC-Ls发生了凋亡。结论姜黄素可通过抑制人微血管内皮细胞增殖、迁移、管样形成并诱导其发生凋亡从而有效抑制肿瘤血管形成，是一种非常具有临床应用前景的抗肿瘤药物。“,” Objective: To study the effects of curcumin on human microvascular endothelial cel (HMVEC-Ls) proliferation, migration, tube formation and apoptosis in vitro. Method:The HMVEC-Ls were treated with different concentrations of curcumin (0, 20, 40 and 80 μmol/L), and HMVEC-Ls proliferation, migration, tube formation and apoptosis were then measured by MTS assay, wound-healing migration assay, Matrigel assay and Hoechst33258 /TUNEL costaining, respectively. Result: The HMVEC-Ls proliferation migration and tube formation was suppressed by curcumin treatment (P<0.05). In contrast, there were significant differences on HMVEC-Ls proliferation at the concentrations of 20, 40 and 80 μmol/L compared with the control group (0 μmol/L) (p<0.05).The HMVEC-Ls migration ratio among the 0, 20 , 40 and 80 μmol/L group were determined to be (92.33±5.01)%, (82.50±5.09)%, (63.00±5.73)%, and (41.00±4.15)%, respectively (p<0.05). Meanwhile, the tube length of HMVEC-Ls among the four experimental group were (2.76±0.14), (1.76±0.09), (0.90±0.16) and (0.34±0.07) mm/field, respectively (p<0.05). In addition, we found the characteristics of apoptosis treated with curcumin at the concentration 80μmol/L. by Hoechst33258 /TUNEL costaining. Conclusion: These findings suggest that curcumin may play pivotal roles in tumor angiogenesis suppression via the inhibition of HMVEC-Ls proliferation, migration, tube formation and promotion of apoptosis.