HECV

MVs Released by Activated Monocytes and Platelets Induce Oxidative Stress in Endothelial Cells

Circulating microvesicles (MVs) have been implicated in endothelial dysfunction, but no study has directly compared platelet- and monocyte-derived MVs. Brambilla et al. aim to assess their involvement in vessel damage processes, including oxidative stress, inflammation, and leukocyte-endothelial adhesion, by evaluating their effects on human vascular endothelial cells (hECV).

Superoxide anion production was measured in endothelial cells exposed to monocyte- (Mo-) and platelet-derived (Plt-) MVs from resting and activated cells. Results show that MVs from resting cells (25-400 MVs/µL) did not affect superoxide production in human vascular endothelial cells (hECV) (Fig. 1A, B). However, LPS-induced Mo-MVs and TRAP-6-induced Plt-MVs significantly increased superoxide production in a concentration-dependent manner, similar to LPS treatment (Fig. 1A, B). This suggests that MVs from resting cells do not alter endothelial redox balance, while those from activated cells have pro-oxidative effects.

Antioxidant Activity of SEE on Dysfunctional Endothelial Cells

Plants are significant sources of bioactive compounds used in functional foods. In the Mediterranean, Sarcopoterium spinosum is traditionally used for weight loss and diabetes treatment. Given the role of inflammation in diseases like cardiovascular conditions, Zbeeb et al. investigated the antioxidant and cytoprotective properties of an ethanolic extract from S. spinosum fruits (SEE) in a cellular model of endothelium dysfunction.

Initially, they tested SEE, single polyphenols (PPs), and H₂O₂ for cytotoxicity on HECV cells. No cytotoxicity was observed for 30 µM H₂O₂, 10 µg/mL SEE, or the PPs corilagin (Cg) and quercetin (Qu) after 24 h (Fig. 2A). Notably, Cg slightly increased cell proliferation. As expected, 30 µM H₂O₂ significantly increased ROS production (+20% vs. control; p ≤ 0.05) (Fig. 2B). Both SEE and PPs significantly reduced ROS levels when administered after (-22% for SEE, -33% for Cg, -22% for Qu) or before (-24% for SEE, -24% for Cg) H₂O₂ exposure. Qu pre-treatment showed no significant effect. Fluorescence microscopy visualized these changes (Fig. 2C). Lipid peroxidation was assessed by measuring malondialdehyde (MDA) using a TBARS assay (Fig. 2D). H₂O₂-insulted cells showed a significant increase in MDA (+63% in protection, +97% in counteraction conditions). In the counteraction condition, all compounds significantly reduced MDA (-110% for SEE, -109% for Cg, -111% for Qu). In the protection condition, SEE and PPs prevented MDA increase (-70% for SEE, -72% for Cg, -64% for Qu). Thus, SEE exhibited strong antioxidant effects, with the counteraction condition being more effective in reducing lipid peroxidation.