Hydroxytyrosol: Its role in the prevention of cardiovascular diseases

Abstract

In recent years, non-pharmacology treatments and their effectiveness have gained popularity due to their beneficial properties in the prevention of cardiovascular diseases. Phenolic compounds intake provides a natural means of improving in vivo antioxidant status. Thus, the purpose of this review is to discuss the potential benefits of hydroxytyrosol (HT), a phenolic compound with powerful antioxidant and anti-inflammatory properties, in preventing and reducing cardiovascular risk factors, concretely atherosclerosis. Closer inspection of the studies showed a significant improvement of lipid profile, antioxidant capacity and inflammatory state. A note of caution is due in vitro studies because the lack of validated approaches difficult the goodness of fit with the in vivo and clinical research. However, animal and clinical studies were very encouraging, determining HT supplementation useful on inflammation, oxidative stress, endothelial function and cardiovascular diseases in general.

Keywords: Atherosclerosis; Hydroxytyrosol; Inflammation; Lipid profile.

Fig. 1

The decrease of nitric oxide (NO) synthesis increases leukocytes and platelets adhesivity. Macrophages uptake oxidized LDL (oxLDL), finally triggering inflammation. OxLDL binds to TLR4 which promote the release of interleukine (IL-6) and monocyte chemotactic protein (MCP-1) among others. As a cycle MCP-1 let monocytes to migrate and infiltrate into subendothelial space differentiating into macrophages by the macrophage colony-stimulating factor (M-CSF). TLR activate the necrosis factor kappa B (NF-kB) pathway leading to udregulation of adhesion molecules (Selectin P and E: adhesion of leukocytes; adhesion molecule-1 [ICAM-1] and vascular adhesion molecule-1 [VCAM-1]: macrophage proliferation) and cytokines (IL-6: express VCAM-1 and ICAM-1, inducting MCP-1 and up taking low-density lipoproteins [LDL]).

Fig. 2

Biological effects of HT on inflammation, oxidative stress and cholesterol pathways. (1) Hydroxytyrosol reduces NF-kB activation causing a depletion at mRNA levels of pro-inflammatory genes such as MCP-1, ICAM-1, VCAM-1, IL-1β, IL-6, TNF-α, E-selectin and P-selectin. (2) In addition, HT pre-treatment rescues SOD activity and reduces lipid peroxide production. Importantly, a positive effect on the mitochondria has been manifested by an increase of the mitochondrial ATP synthase activity. (3) Moreover, the expression of ABCA1, a transporter enrolled in cholesterol homeostasis (HDL-chol synthesis), is increased after HT treatment. (4) Finally, Akt1 activation by HT improved the NO levels in endothelial cells.