中文摘要：

【目的】研究姜黄素对人微血管内皮细胞（HMVEC-L）增殖、迁移、成管以及凋亡的影响。【方法】将姜黄素分为0、20、40、80／＆mol／L4个实验组，分别用非放射性细胞增殖检测（MTS）法、划痕实验、成管实验以及Hoechst 33258与TUNEL双重荧光法检测姜黄素对HMVEC-L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-L共同培养的第1天开始，20～80μmol／L浓度组均可抑制HMVEC-L增殖．与对照纽（0μmol／C）比较差异有统计学意义（P〈0．05或P〈0．01），尤以80μmol／L组抑制HMVEC-L增殖能力最显著（P〈0．05或P〈0．01）。划痕实验结果显示：20～80μmol／L姜黄素浓度组HMVEC-L迁移率均显著降低．各组HMVEC-L迁移率比较差异有统计学意义（P〈0．05）．其中尤以80μmol／L组HMVEC-L迁移率最低。成管实验结果显示：20～80μmol／L姜黄素浓度组HMVEC-L成管长度均显著降低．各组HMVEC-L成管长度比较差异有统计学意义（P〈0．05），其中尤以80μmol／L组HMVEC-L成管长度最小。Hoechst 33258与TUNEL双重荧光染色结果显示：在姜黄素与HMVEC～L共同培养过程中HMVEC-L发生了凋亡。【结论】姜黄素可通过抑制HMVEC-L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。

英文摘要：

Objective To study the effect of curcumin on the proliferation, migration, tube formation and apoptosis of human lung microvascular endothelial cells （HMVEC-L） in vitro. Methods The HMVEC-L were co-cultured with different concentrations of curcumin （0, 20, 40 and 80 μmol/L） , and then HMVEC-L proliferation, migration, tube formation and apoptosis were measured by non-radioactive MTS/PES assay, scratch adhesion test, Matrigel assay and Hoechst33258/TUNEL fluorescence staining, respectively. Results The results of non-radioactive MTS/PES assay showed that HMVEC-L proliferation was suppressed by 20 - 80μmol/L of curcumin, in particular by 80 μmol/L of eurcumin, from the first day of co-cuhure （P〈0.05 or P〈0.01 compared with the control group at 0 μmol/L） The results of scratch adhesion test showed that HMVEC-L migration rate was decreased by 20- 80 μmol/L of curcumin （P〈0.05）, and the rate was the lowest in curcumin group of 80 μmol/L. The co-culture of curcumin at 20 - 80 μmol/L also reduced the length of formative tube of HMVEC-L, and the effect of 80μmol/L of curcumin was the strongest （P〈0.05） Matrigel assay and Hoechst33258 /TUNEL fluorescence staining showed that migration and tube formation was suppressed by curcumin treatment, and the apoptosis of HMVEC-L was presented after the co-culture with curcumin. Conclusion Curcumin may play the role of tumor angiogenesis suppression through the inhibition of HMVEC-L proliferation, migration, tube formation and apoptosis.