AIM: To observe the effects of different concentrations of curcumin on the proliferation and expression of VEGF and NF-κB p65 of human retinal capillary endothelial cells(HRCECs)induced by high glucose in vitro.

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.