Role of mitochondrial apoptosis pathway in palmitic acid-induced cell apoptosis in vascular endothelial cells / 中国药理学通报

ABSTRACT

Aim: To explore the role of mitochondrial apoptosis pathway in palmitic acid (PA) -induced cell apoptosis in human umbilical vein endothelial cells (HUVECs). Methods: HUVECs were exposed to different concentrations of PA (0. 1, 0. 2, 0. 4, 0. 8 mmol · L-1) for 24 h and different time points of 0.4 mmol · L-1 PA (0, 12, 24, 48 h). Cell viability was measured by MTT. The expression of reactive oxygen species (ROS) in HUVECs was detected by immunofluorescence. The level of intracellular apoptosis was detected by TUNEL assay. The protein expressions of mitochondrial apoptosis pathway proteins such as AIF, Cyt-C, cleaved caspase-3, Bcl-2, Bax were determined by Western blot. Results: HUVECs exposed to PA at 0. 4 mmol · L-1 for 24 h showed a decrease in their viability and an increase in the level of AIF, Cyt- C, cleaved caspase-3, Bax/Bcl-2 (P < 0. 05). Cell apoptosis level was significantly up-regulated (P < 0. 05). The intracellular apoptosis levels in the vascular endothelial cells treatment with mitochondrial apoptosis pathway inhibitor ciclosporine A (CsA) were significantly lower than those of PA group (P < 0. 05). Conclusion: Activated mitochondrial apoptosis pathway might play an important role in PA-induced cell apoptosis in vascular endothelial cells.