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• W2327589969 abstract "Objective The mechanisms by which oxidized low-density lipoprotein (ox-LDL) induces the expression of adhesion molecules on endothelial cells (HUVECs) are still not clear. The signal transduction pathways for these binding molecules include the translocation of the transcription factor NF-kB and the intracellular reactive oxygen species (ROS) are said to play a key role in this process. Aim of this study was (1) to evaluate the effect of ox-LDL on intracellular production of ROS in culture of HUVECs; (2) to evaluate if the intracellular increase of ROS induced by ox-LDL is mediated by the binding to a specific endothelial receptor; (3) to ascertain if lacidipine can decrease ox-LDL-induced ROS production in HUVECs. Methods Five *MCu2 + ox-LDL were incubated with HUVECs for 5 min. 2′,7′-Dichlorofluorescein (DCF) as an expression of intracellular ROS production, was measured by flow cytometry. Results ox-LDL induced a significant dose-dependent increase in DCF production (P < 0.001) through the binding to a specific receptor. The preincubation of HUVECs with radical scavengers compounds and lacidipine significantly reduced (P < 0.001) the ox-LDL-induced DCF production. Conclusions ox-LDL increased the intracellular formation of ROS through the ligation to a specific endothelial receptor. Preincubation of HUVECs with lacidipine, a calcium antagonist with antioxidant properties, significantly reduced the intracellular ROS formation induced by ox-LDL. We propose that the effect of lacidipine on adhesion molecule expression and on NF-kB activation can be explained by its effect on intracellular ROS formation." @default.
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• W2327589969 date "1998-12-01" @default.
• W2327589969 modified "2023-09-23" @default.
• W2327589969 title "Oxidized low-density lipoprotein increases the production of intracellular reactive oxygen species in endothelial cells" @default.
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• W2327589969 doi "https://doi.org/10.1097/00004872-199816121-00010" @default.
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