Does autophagy play a key role in the protective effect of oleic acid against oxidative stress in endothelial cells?

Oxidative stress has been proposed as a mechanism that provokes endothelial dysfunction, which is the primary cause of cardiovascular complications involved in the pathogenesis of atherosclerosis. Thus, prevention of oxidative stress is a strategy to avoid endothelial dysfunction and cardiovascular disease. Since oleic acid has been shown to have a chemoprotective effect on endothelial cells against induced oxidative stress by reducing reactive oxygen species, we evaluated other potential cellular mechanisms that could be responsible for this protective effect. Autophagy is considered a cellular adaptive response under stressful conditions; thus, its role in the protective mechanism of oleic acid in stressed endothelial (EA.hy926) cells was assessed. To that end, we evaluated cell viability and markers of oxidative status, such as reactive oxygen species, reduced glutathione, glutathione peroxidase and reductase. Moreover, we investigated the expression of several key autophagy-related proteins, such as microtubule-associated protein 1 light chain 3 beta and ubiquitin-binding protein p62/sequestosome 1. The results showed that oleic acid within the micromolar range stimulated autophagy. However, when autophagy is inhibited in endothelial cells under oxidative stress, the chemoprotective effect of oleic acid is minimal. These results suggest a limited contribution of autophagy to the protective effect of oleic acid under conditions of severe oxidative stress.