To study the effect of curcumin on the growth properties of circulating endothelial progenitor cells

Abstract

Curcumin has been shown to regulate the expression of genes implicated in tumor cell proliferation, metastasis, chemotherapy resistance, and angiogenesis. Endothelial progenitor cells (EPCs) have been recently described in the peripheral blood as cells contributing to both physiological and pathological angiogenesis. In the current study, we evaluated the effect of curcumin on these angiogenic cells. EPCs were isolated, expanded, and characterized ex vivo. These cells were then treated with different concentrations of curcumin. The formation of EPC colonies in culture and their proliferation was analyzed by 5'-bromo-2'-deoxyuridine assays in absence and presence of curcumin. Further, the expression of two important cell cycle inhibitory proteins, p21 and p53, in the curcumin- and culture medium-treated cells without curcumin was evaluated by intracellular flow cytometry. The results showed that there was a significant decrease in the formation of EPC colonies in culture. EPC proliferation was significantly inhibited by curcumin in a dose-dependent manner. Flow cytometry analysis showed a twofold increase in the expression of both p21 and p53 in curcumin-treated cells as compared to the medium-treated cells, suggesting that curcumin inhibits EPC growth by mainly inhibiting the G1 to S phase transition in the cell cycle. It would be further worthwhile to study the effect of curcumin on EPC-mediated angiogenic activity.

Inflammation and dysfunction in human aortic endothelial cells associated with poly‐l‐lactic acid degradation in vitro are alleviated by curcumin

“…Here, 12.5% PLLA and 5 μM Cur had mild cytotoxicity (cell viability>50%) and were selected for subsequent assays to avoid the interference of non-specific injury responses by cell necrosis. As Monfoulet et al reported that Cur modulates the expression of 15 genes involved in the control of the cytoskeleton and endothelial junction dynamics (Vyas, Gupt, Dixit, Anita, & Kaur, 2015); this study further demonstrated that Cur improved the healing rate of HAEC treated with PLLA, which may be due to the modulation of migration and growth properties (Deanfield, Halcox, & Rabelink, 2007). Additionally, cell migration enhanced by Cur could help form the endothelial monolayer, which prevents the occurrence of thrombosis (Sethi, Sung, & Aggarwal, 2008).…”