Unhealthy lifestyles have placed a significant burden on individuals' cardiovascular health. Anthocyanins are water-soluble flavonoid pigments found in a wide array of common foods and fruits. Anthocyanins have the potential to contribute to the prevention and treatment of cardiovascular disease by improving lipid profiles and vascular function, reducing blood glucose levels and blood pressure, and inhibiting inflammation. These actions have been demonstrated in numerous clinical and preclinical studies. At the cellular and molecular level, anthocyanins and their metabolites could protect endothelial cells from senescence, apoptosis, and inflammation by activating the phosphoinositide 3-kinase/protein kinase B/endothelial nitric oxide synthases, silent information regulator 1 (SIRT1), or nuclear factor erythroid2-related factor 2 pathways and inhibiting the nuclear factor kappa B, Bax, or P38 mitogen-activated protein kinase pathways. Furthermore, anthocyanins prevent vascular smooth muscle cell from platelet-derived growth factor -induced or tumor necrosis factor-α-induced proliferation and migration by inhibiting the focal adhesion kinase and extracellular regulated protein kinases signaling pathways. Anthocyanins could also attenuate vascular inflammation by reducing the formation of oxidized lipids, preventing leukocyte adhesion and infiltration of the vessel wall, and macrophage phagocytosis of deposited lipids through reducing the expression of cluster of differentiation 36 and increasing the expression of ATP-binding cassette subfamily A member 1 and ATP-binding cassette subfamily G member 1. At the same time, anthocyanins could lower the risk of thrombosis by inhibiting platelet activation and aggregation through down-regulating P-selectin, transforming growth factor-1, and CD40L. Thus, the development of anthocyanin-based supplements or derivative drugs could provide new therapeutic approaches to the prevention and treatment of vascular diseases.
Keyphrases
- nuclear factor
- signaling pathway
- oxidative stress
- protein kinase
- toll like receptor
- growth factor
- blood glucose
- blood pressure
- cardiovascular disease
- nitric oxide
- transforming growth factor
- water soluble
- smooth muscle
- diabetic rats
- poor prognosis
- endothelial cells
- epithelial mesenchymal transition
- binding protein
- high glucose
- induced apoptosis
- healthcare
- drug induced
- public health
- tyrosine kinase
- rheumatoid arthritis
- dna damage
- stem cells
- biofilm formation
- type diabetes
- ms ms
- pi k akt
- cell death
- endoplasmic reticulum stress
- adipose tissue
- skeletal muscle
- staphylococcus aureus
- fatty acid
- health information
- high resolution
- mesenchymal stem cells
- cell proliferation
- mass spectrometry
- hypertensive patients
- pseudomonas aeruginosa
- dna binding
- amino acid
- cystic fibrosis
- bone marrow
- stress induced
- case control