Citreoviridin inhibits cell proliferation and enhances apoptosis of human umbilical vein endothelial cells

• We investigated the effects of CIT on apoptosis and proliferation of human umbilical vein endothelial cells (HUVECs).
• CIT inhibited HUVECs proliferation and the cells were arrested at G0/G1 phase, which is associated with decreased levels of cyclinD1 and increased expression of p53 and p21.
• CIT-induced apoptosis was accompanied by the activation of caspase-3, -9.

In some areas of China, citreoviridin (CIT) is considered one of the risk factors for development of cardiovascular disease (CVD). Apoptosis of endothelial cell may induce vascular endothelium injury and atherosclerosis, which result in CVD probably. In this study, we investigated the effect of CIT on apoptosis and proliferation of human umbilical vein endothelial cells (HUVECs). The MTT assay was used to determinate HUVECs proliferation. Distribution of the cell cycle was analyzed by flow cytometry. The Annexin-V/PI staining was used to investigate cell apoptosis. Western blotting analysis was used to indicate changes in the expression level of apoptosis-related proteins. The results indicated that CIT inhibited HUVECs proliferation and the cells were arrested at G0/G1 phase, which is associated with decreased levels of cyclinD1 and increased expression of p53 and p21. The apoptosis rate of HUVECs was improved by CIT. The expression of Bcl-2 were down-regulated after CIT treatment, whereas the levels of Bax was significantly up-regulated. Furthermore, CIT-induced apoptosis was accompanied by the activation of caspase-3, -9. These findings demonstrate that CIT inhibits cell proliferation via DNA synthesis reduction and induces caspase-dependent apoptosis in HUVECs. CIT plays a pivotal role in the process of endothelial cell apoptosis, may thereby play an important role in the improvement of CVD in areas of China that have a high prevalence of CIT contamination.