The protective effect of hydroxytyrosol on cardiovascular diseases

Hydroxytyrosol, a natural polyphenolic compound derived from olives, has been confirmed to exert protective effects on the cardiovascular system in numerous basic and preclinical studies. Its mechanisms involve multiple aspects such as antioxidation, anti-inflammation, regulation of lipid metabolism, and improvement of vascular function, as detailed below:

I. Core Protective Effects on Cardiovascular Diseases

The protective effects of hydroxytyrosol are mainly reflected in the prevention and improvement of common cardiovascular diseases such as atherosclerosis, hypertension, and myocardial injury:

In terms of atherosclerosis, it can delay lipid deposition and plaque formation in the vascular wall, reducing the risk of vascular stenosis;

For hypertension, it can assist in lowering blood pressure by regulating vascular tone;

For conditions such as myocardial ischemia-reperfusion injury or myocardial hypertrophy, hydroxytyrosol can alleviate oxidative stress and inflammatory responses in myocardial cells, improving myocardial function.

II. Key Mechanisms of Protective Effects

Antioxidative Damage and Reduction of Vascular Oxidative Stress

Vascular endothelial cells, when chronically exposed to oxidative stress (e.g., excessive free radicals), undergo endothelial dysfunction, which is the initial step of cardiovascular diseases. Hydroxytyrosol exerts antioxidant effects through two pathways:

Directly scavenging reactive oxygen species (such as superoxide anions and hydrogen peroxide) to reduce free radical-induced damage to vascular endothelium;

Upregulating the activity of endogenous antioxidant enzymes (e.g., superoxide dismutase, glutathione peroxidase) to enhance the body’s own antioxidant system, reduce the production of lipid peroxidation products (e.g., malondialdehyde), and thus protect the structural and functional integrity of vascular endothelium.

Inhibition of Inflammatory Responses and Blocking of Chronic Vascular Inflammation

Chronic inflammation is a core driver of the progression of cardiovascular diseases like atherosclerosis. Hydroxytyrosol can inhibit the release of pro-inflammatory factors (e.g., tumor necrosis factor-α, interleukin-6) by regulating inflammatory signaling pathways (such as the NF-κB pathway), reducing the infiltration and aggregation of inflammatory cells (e.g., monocytes, macrophages) in the vascular wall, thereby preventing inflammatory damage and plaque formation in the vascular wall. Additionally, it can downregulate the expression of adhesion molecules (e.g., intercellular adhesion molecule-1), reducing the adhesion of leukocytes to vascular endothelium and further alleviating vascular inflammation.

Regulation of Lipid Metabolism and Improvement of Lipid Profiles

Dyslipidemia (e.g., high cholesterol, high low-density lipoprotein cholesterol) is a significant risk factor for cardiovascular diseases. Hydroxytyrosol can promote the conversion and excretion of cholesterol into bile acids by affecting the activity of cholesterol metabolism-related enzymes (e.g., cholesterol 7α-hydroxylase), reducing serum total cholesterol levels. Meanwhile, it can inhibit the oxidative modification of low-density lipoprotein (LDL) — oxidized LDL is a key pathogenic factor in atherosclerosis — reduce foam cell formation, and delay lipid deposition in the vascular wall.

Improvement of Vascular Function and Maintenance of Vascular Tone

Vascular endothelial dysfunction leads to decreased vasodilatory capacity and vascular spasm, which can further trigger hypertension or myocardial ischemia. Hydroxytyrosol can promote vascular endothelial cells to release nitric oxide (NO), an important vasodilator factor. By activating guanylate cyclase, it increases cGMP levels in vascular smooth muscle cells, causing vascular smooth muscle relaxation, improving vascular elasticity, and enhancing blood perfusion. Additionally, it can inhibit the production of vasoconstrictive factors (e.g., endothelin-1), balance vascular vasomotor function, and maintain normal blood pressure.

Inhibition of Platelet Aggregation and Prevention of Thrombosis

Thrombosis is a major trigger of severe cardiovascular events such as acute myocardial infarction and cerebral infarction. Hydroxytyrosol can reduce the production of thromboxane A₂ (a potent platelet aggregator) by inhibiting arachidonic acid metabolism on platelet membranes, while enhancing the effect of prostaglandin I₂ (a factor that inhibits platelet aggregation). This reduces platelet aggregability and lowers the risk of thrombosis.

III. Summary and Outlook

Hydroxytyrosol exerts comprehensive protective effects on the cardiovascular system through multi-target mechanisms including antioxidation, anti-inflammation, lipid regulation, improvement of vascular function, and inhibition of thrombosis. Its natural origin gives it great potential for application in the prevention and auxiliary treatment of cardiovascular diseases. However, most current studies are still based on animal models or in vitro experiments, and clinical studies (especially large-sample population studies) are relatively limited. Future research should further explore its dose-effect relationship in humans and the safety of long-term application to promote its clinical translation in the prevention and treatment of cardiovascular diseases.