Figure 3. Curcumin inhibits growth, proliferation, migration and tube formation in human intestinal microvascular endothelial cells (HIMECs). (A) Potent angiogenic effect of vascular endothelial growth factor (VEGF) compared with no stimulation in HIMECs. Curcumin inhibited HIMEC growth at rates almost similar to those of control cells. The cyclo-oxygenase-2 (COX-2) inhibitor, NS398 was a potent inhibitor of cell growth. (B) Cellular DNA synthesis was assessed by measuring [3H]thymidine uptake. [3H]Thymidine uptake was significantly increased after VEGF stimulation for 15 h and was inhibited by curcumin pretreatment for 30 min in a dose-dependent manner. Assays were done in triplicate and the data are shown as mean cpm (SD). *p<0.05 compared with VEGF-stimulated HIMEC cultures. (C) The inhibitory effect of curcumin on [3H]thymidine uptake was reversed by addition of carbacyclin (a prostaglandin I2 (PGI2) analogue). *p<0.05 compared with curcumin-treated HIMECs with no exogenous PG. (D) The number of HIMECs transmigrated through the filter was increased by VEGF stimulation; curcumin pretreatment of HIMECs significantly inhibited HIMEC transmigration, which was reversed by 1 μM carbacyclin. At least 15 random high-power fields (×200) per condition were counted and data were expressed as mean (SD). *p<0.05 compared with curcumin pretreatment. (E) Phase-contrast photomicrograph demonstrates the endothelial in vitro tube formation on Matrigel; the formation of capillary-like structures was inhibited by curcumin pretreatment (×40).
