Serum of coronary atherosclerotic heart disease patients induces oxidative stress injury on endothelial cells

Abstract

Endothelial cell (EC) dysfunction has a fundamental role in the development of atherosclerosis, which leads to myocardial infarction and stroke. The aim of this study is to investigate the effect of serum from patients with coronary atherosclerotic heart disease (CAD) on endothelial cells and investigate the possible mechanism underlying these effects. Serum from 35 patients with CAD and 35 healthy volunteers was collected. Human umbilical vein endothelial cell (HUVEC) proliferation and apoptosis were assessed by a CCK‑8 assay and a flow cytometry assay, respectively. The synthesis of nitric oxide (NO) and reactive oxygen species (ROS) was measured using the nitrate reduction method and DCFH2-DA staining, respectively. The proliferation of HUVECs was inhibited by treatment with serum from CAD patients (P<0.05). Suppression of HUVEC proliferation by CAD serum occurred in a concentration-dependent manner. The synthesis of NO was also reduced in the CAD serum-treated group. Furthermore, the serum from CAD patients increased both apoptosis and intracellular ROS production in HUVECs. Moreover, treatment with tempol antagonized CAD serum-meditated HUVEC injuries. Taken together, these results suggest that HUVEC injury via CAD serum treatment is mediated by ROS production. Tempol may partly reverse this effect by abolishing HUVEC apoptosis.

Proteomic profiling for prediction of recurrent cardiovascular event in patients with acute coronary syndrome and obstructive sleep apnea: A post-hoc analysis from the ISAACC study

“…OSA was found to be related to oxidative stress, by increasing the synthesis of reactive oxygen species [8,34,35]. At the same time, this increase entails the development of atherosclerosis, which stimulates vascular endothelial cell structural damage and dysfunction [36]. In addition, OSA was also related to inflammation in different aspects [35,37,38].…”

“…These three proteins are widely described as cardiovascular risk factors. CXCL16 plays an important role in atherosclerosis and plaque destabilization [36,44,45]. STK4 is a key component of the Hippo signaling pathway and is thus an essential regulator of cardiac development and regeneration/repair after injury [46,47].…”