The Mechanism Of Palmitic Acid Promoting Endothelial Progenitor Cells' Apoptosis

Objective: To study the effects of palmitic acid(PA)on apoptosis of endothelial progenitor cells (EPC) and its molecular mechanism.Methods: The mononuclear cells were obtained by Ficoll density gradient centri- fugation and induced into EPC in vitro. After stimulated with PA, the expression of caspase-3 and the influence of mitogen activated protein kinase (MAPK) inhibitors, TXL on caspase-3 expression were observed by Western blot. Flow cytometry was used to detect the apoptosis of EPC. The activity of caspase-3 protein and secretion cytokines were measured by ELISA.The activity of ROS was measured by fluorescence microscope. Then the intervet affection of TXL was observed.Results: PA increases EPC apoptosis in a dose and time-dependent manner, PA also up-regulate the expression and activity of caspase-3, secretion of TNF-αand activity of ROS, thus these effects can be inhibited by p38 MAPK inhibitor SB203580, Jnk-MAPK inhibitor SP600125 and TXL.Conclusion: PA increases the apoptosis of EPC and up-regulates the expression and activity of caspase-3, secretion of TNF-αand activity of ROS, partly through p38, Jnk MAPK pathway; and those influence can partly be infinited by p38, Jnk- MAPK inhibitor and TXL. These findings might explain in part the interactive roles of PA and EPC in the processes of atherosclerosis and intervent affection of TXL.