Rb1 restores palmitic acid-induced reduction of Ca2+ influx by activating PLC in EA cells and PLD in MOVAS cells

초록

Recent interest has focused on the role of Ca2+ in regulating health problems, including cardiovascular disease and colorectal cancer. The inverse correlation between colon cancer and serum Ca2+ underlines the importance of understanding intracellular Ca2+ dynamics. Studies are also evaluating the contributions of abnormalities in Ca²⁺ homeostasis and intracellular dysfunction to the pathogenesis of metabolic syndrome as a precursor of cardiovascular disease. In this study, we investigated the changes of Ca2+ dynamics and ginsenoside Rb1 (Rb1)-induced recovery in two vascular cell lines exposed to palmitic acid (PA), the most abundant active ingredient in palm oil. The mechanism underlying the Rb1-induced recovery was examined in a store operated Ca2+ entry model by Ca2+ store depletion. PA reduced the Ca2+ influx in both EA.hy926 (EA) and MOVAS cells, and this change was restored by Rb1. In EA cells, the Rb1-induced restoration was abolished by U73122 or 2-APB. In MOVAS cells, meanwhile, the effect of Rb1 was abolished by FIPI, U73122 and U73343. Under normal conditions, Rb1 itself altered phospholipid signaling (PLC in EA cells and PLD in MOVAS cells), but did not affect Ca2+ homeostasis. These differences resulted in differences in downstream actions, as KB-R7943 and nifedipine inhibited Rb1-mediated Ca2+ influx recovery only in MOVAS cells. In conclusion, Rb1 rescues the PA-induced Ca2+ influx by appropriately activating PLC in EA cells and PLD in MOVAS cells. This demonstrates that Ca2+ dynamics are elaborately regulated via intracellular Ca2+ signaling networks, suggesting a potential strategy for maintaining vascular Ca2+ homeostasis in hyperlipidemic environments. © 2025 The Authors

키워드