方法：用高糖培养基模拟糖尿病环境建立HRCECs体外高糖模型，将培养的细胞分为：正常对照组、高糖对照组、高糖+20、40、80μmol/L姜黄素组，分别用CCK-8法检测姜黄素干预后HRCECs的增殖能力，用Western-blot及免疫细胞化学法检测VEGF、NF-κB p65的表达。

结果：CCK-8法结果示：与正常对照组比较，高糖显著促进HRCECs增殖(P<0.01)，各浓度姜黄素作用12、24、48h后与高糖对照组比较，细胞增殖均有明显抑制作用(P<0.01)，且呈浓度与时间依赖性。Western-blot结果示：与正常对照组比较，高糖对照组中VEGF-A、NF-κB p65表达显著增加(P<0.01)，各浓度姜黄素作用12、24、48h后与高糖对照组比较，VEGF-A、NF-κB p65的表达显著减少，且随着浓度增加、时间延长抑制作用增强，各加药组间两两比较均有差异(P<0.01)。免疫细胞化学法结果示：与正常对照组相比，高糖对照组VEGF表达显著增加(P<0.01)，各浓度姜黄素干预24h后与高糖对照组比较，VEGF表达逐渐下降(P<0.01)，各加药组间两两比较均有差异(P<0.01)。

结论：姜黄素可呈浓度与时间依赖性地抑制高糖诱导的HRCECs增殖以及VEGF、NF-κB p65的表达，这种增殖抑制作用可能与其下调VEGF、NF-κB p65表达有关。

METHODS: The hyperglycemia model of HRCECs in vitro was established by simulating diabetic environment with high glucose medium. The cultured cells were divided into normal control group, high glucose control group, high glucose + 20, 40 and 80μmol/L curcumin groups. The proliferation of HRCECs was detected by CCK-8 assay, and the expression of VEGF and NF-κB p65 was detected by Western-blot and immunocytochemistry.

RESULTS: The results of CCK-8 assay showed that high glucose promoted the proliferation of HRCECs significantly compared with the normal control group(P<0.01). Curcumin at different concentrations could inhibit the proliferation of cells significantly in a concentration-dependent and time-dependent manner compared with the high glucose control group after being treated with curcumin at different concentrations for 12, 24 and 48h(P<0.01). The results of Western-blot showed that compared with the normal control group, the expression of VEGF-A and NF-κB p65 in the high glucose control group was increased significantly(P<0.01). Compared with the high glucose control group, the expression of VEGF-A and NF-κB p65 decreased significantly after being treated with curcumin at different concentrations for 12, 24 and 48h, and positively correlated with concentration and time(P<0.01). The results of immunocytochemistry showed that the expression of VEGF in the high glucose control group was significantly higher than that in the normal control group(P<0.01). After 24h of treatment with curcumin,the expression of VEGF was gradually decreased compared with the high glucose control group(P<0.01). There were significant differences in pairwise comparison between each group(P<0.01).

CONCLUSION: Curcumin can inhibit the proliferation and the expression of VEGF and NF-κB p65 of HRCECs induced by high glucose in a concentration-dependent and time-dependent manner, which may be related to its down-regulation of the expression of VEGF and NF-κB p65.