BACKGROUND: This study aimed to investigate the inhibitory effect of blueberry anthocyanin (BBA) on Angiotensin II (Ang II)-induced apoptosis of human umbilical vein endothelial cells (HUVECs), and its regulation mechanisms involving Bax and Caspase 3.

MATERIAL AND METHODS: HUVECs were first treated by different concentrations of Ang II (10–9, 10–8, 10–7, 10–6, 10–5, and 10–4 mol/L) and BBA (80, 40, 20, 10, 5, and 2.5 μg/ml). After 24 h and 48 h of treatment, MTT was performed to detect the viability of HUVECs. Then, HUVECs were randomly divided into the Ang II group (10–6 mol/L Ang II) and Ang II + BBA group (10–6 mol/L Ang II and 20 μg/ml BBA), and the apoptosis rate was detected by flow cytometry. Western blot analysis was performed to detect the expression of Bax and Caspase 3 in these 2 groups. During the whole process, HUVECs without any treatments served as the control group.

RESULTS: The cell viability of HUVECs was significantly reduced by Ang II in a time- and concentration-dependent manner (P<0.05), while BBA significantly elevated the cell viability of HUVECs until a peak of 20.0 μg/ml. The apoptosis rate of HUVECs was significantly increased by Ang II (P<0.01) and reduced by the BBA intervention (P<0.05). Ang II significantly elevated the expression of Bax and Caspase 3 in HUVECs, but their expression was significantly inhibited by BBA.

CONCLUSIONS: BBA increased cell viability and reduced apoptosis rate of HUVECs induced by Ang II through Bax- and Caspase 3-dependent pathways.

Keywords: Anthocyanins - pharmacology, Angiotensin II - toxicity, Blueberry Plants - chemistry, Cell Survival - drug effects, Human Umbilical Vein Endothelial Cells, Nitric Oxide Synthase Type III - metabolism, Random Allocation, Reactive Oxygen Species - metabolism, Signal Transduction - drug effects, bcl-2-Associated X Protein - metabolism