Abstract
Atherosclerotic cardiovascular disease is linked to both oxidative stress and endothelial cell dysfunction. Chicoric acid has antioxidant and anti-inflammatory properties. In the present investigation, we demonstrated that chicoric acid inhibits oxidized low-density lipoprotein (oxLDL)-facilitated dysfunction in human umbilical vein endothelial cells (HUVECs). Oxidative injuries were tested by investigating the formation of intracellular reactive oxygen species (ROS) and by examining the activity of antioxidant enzymes and the function of endothelial nitric oxide synthase (eNOS). We also confirmed that chicoric acid mitigates apoptotic features caused by oxLDL, such as the subsequent break down of mitochondrial transmembrane potential and the activation of Bax, which promote DNA strand breaks and activate caspase-3. Moreover, our data revealed that chicoric acid attenuated the oxLDL activation of NF-?B, the attachment of THP-1 cells and the overexpression of adhesion molecules in human endothelial cells. The results of this study suggest a potential molecular mechanism through which chicoric acid inhibits oxLDL-induced human endothelial dysfunction.
Highlights
Atherosclerotic damage is linked to oxidative injuries [1]
OxLDL reduced superoxide dismutase (SOD) and catalase activity in 24h treatment. This result suggested that oxidized low-density lipoprotein (oxLDL)-induced reactive oxygen species (ROS) formation may the up-stream signaling in regulation of cell death and antioxidant enzymes dysfunction
Chicoric acid inhibited the production of ROS, which subsequently inhibited the function of both SOD and catalase, promoted the bioavailability of NO and maintained the mitochondrial membrane, thereby preventing pro-apoptotic responses in oxLDL-treated endothelial cells
Summary
Atherosclerotic damage is linked to oxidative injuries [1]. The initial stages of atherosclerosis are facilitated by the augmentation of oxidized low-density lipoprotein (oxLDL) and the aggregation of vascular cells. The subsequent overexpression of adhesion molecules and enhanced adherence of monocytes to endothelial cells were shown as important events in the progression of atherosclerosis [2, 3]. High doses of ROS can cause cell dysfunction and death via the oxidation-induced modification of proteins, nucleic acids, carbohydrates and lipids. Those modifications regulate endothelial inflammatory responses and apoptotic events [7]. Adhesion molecules are thought to be early indicators of atherosclerosis [13] For this reason, therapeutic strategies involving inhibitors of oxLDL-mediated endothelial dysfunction may reduce the progression of atherosclerotic pathology, inhibit their morbidity and promote the survival of patients with cardiovascular diseases
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