Effects of chlorogenic acid on intracellular calcium regulation in lysophosphatidylcholine-treated endothelial cells
2017
Jung, H.J., Keimyung University School of Medicine, Daegu, Republic of Korea | Im, S.S., Keimyung University School of Medicine, Daegu, Republic of Korea | Song, D.K., Keimyung University School of Medicine, Daegu, Republic of Korea | Bae, J.H., Keimyung University School of Medicine, Daegu, Republic of Korea
Lysophosphatidylcholine (LPC) is a major phospholipid component of oxidized low-density lipoprotein (ox-LDL) and is implicated in its atherogenic activity. This study investigated the effects of LPC on cell viability, intracellular calcium homeostasis, and the protective mechanisms of chlorogenic acid (CGA) in human umbilical vein endothelial cells (HUVECs). LPC increased intracellular calcium ([Ca²+]i) by releasing Ca²+ from intracellular stores and via Ca²+ influx through store-operated channels (SOCs). LPC also increased the generation of reactive oxygen species (ROS) and decreased cell viability. The mRNA expression of Transient receptor potential canonical (TRPC) channel 1 was increased significantly by LPC treatment and suppressed by CGA. CGA inhibited LPC-induced Ca²+ influx and ROS generation, and restored cell viability. These results suggested that CGA inhibits SOC-mediated Ca²+ influx and ROS generation by attenuating TRPC1 expression in LPC-treated HUVECs. Therefore, CGA might protect endothelial cells against LPC injury, thereby inhibiting atherosclerosis.
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