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How Flavonoids Prevent Cardiovascular Disease and (2009/1/16 15:16:20)

Definition:

Flavonoids are a large family of compounds synthesized by plants. Over the past decade, scientists have become increasingly interested in the potential for various dietary flavonoids to explain some of the health benefits associated with fruit- and vegetable-rich diets. The hypothesis that dietary flavonoids promote health and prevent disease in humans.

Effects on Cell-Signaling Pathways

Cells are capable of responding to a variety of different stresses or signals by increasing or decreasing the availability of specific proteins. The complex cascades of events that lead to changes in the expression of specific genes are known as cell-signaling pathways or signal transduction pathways. These pathways regulate numerous cell processes, including growth, proliferation, and death. Although it was initially hypothesized that the biological effects of flavonoids would be related to their antioxidant activity, available evidence from cell culture experiments suggests that many of the biological effects of flavonoids are related to their ability to modulate cell-signaling pathways. Intracellular concentrations of flavonoids required to affect cell-signaling pathways are considerably lower than those required to affect cellular antioxidant capacity. Flavonoid metabolites may retain their ability to interact with cell-signaling proteins even if their antioxidant activity is diminished. Effective signal transduction requires proteins known as kinases that catalyze the phosphorylation of target proteins at specific sites. Cascades involving specific phosphorylations or dephosphorylations of signal transduction proteins ultimately affect the activity of transcription factors—proteins that bind to specific response elements on DNA and promote or inhibit the transcription of various genes. The results of numerous studies in cell culture suggest that flavonoids may affect chronic disease by selectively inhibiting kinases. Cell growth and proliferation are also regulated by growth factors that initiate cell-signaling cascades by binding to specific receptors in cell membranes. Flavonoids may alter growth factor signaling by inhibiting receptor phosphorylation or blocking receptor binding by growth factors.

Modulation of cell-signaling pathways by flavonoids could help prevent cancer by:

Stimulating phase II detoxification enzyme activity: Phase II detoxification enzymes catalyze reactions that promote the excretion of potentially toxic or carcinogenic chemicals.

Preserving normal cell cycle regulation: Once a cell divides, it passes through a sequence of stages collectively known as the cell cycle before it divides again. Following DNA damage, the cell cycle can be transiently arrested at damage
checkpoints, which allows for DNA repair or activation of pathways leading to cell death (apoptosis) if the damage is irreparable. Defective cell cycle regulation may result in the propagation of mutations that contribute to the development
of cancer.

Inhibiting proliferation and inducing apoptosis: Unlike normal cells, cancer cells proliferate rapidly and lose the ability to respond to cell death signals that initiate apoptosis.

Inhibiting tumor invasion and angiogenesis: Cancerous cells invade normal tissue aided by enzymes called matrix-metalloproteinases. To fuel their rapid growth, invasive tumors must develop new blood vessels by a process known as
angiogenesis.

Decreasing inflammation: Inflammation can result in locally increased production of free radicals by inflammatory enzymes, as well as the release of inflammatory mediators that promote cell proliferation and angiogenesis and inhibit
apoptosis.

Modulation of cell-signaling pathways by flavonoids could help prevent cardiovascular disease by:

Decreasing inflammation : Atherosclerosis is now recognized as an inflammatory disease, and several measures of inflammation are associated with increased risk of myocardial infarction (heart attack).

Decreasing vascular cell adhesion molecule expression: One of the earliest events in the development of atherosclerosis is the recruitment of inflammatory white blood cells from the blood to the arterial wall. This event is dependent on the expression of adhesion molecules by the vascular endothelial cells that line the inner walls of blood vessels.

Increasing endothelial nitric oxide synthase (eNOS) activity: eNOS is the enzyme that catalyzes the formation of nitric oxide by vascular endothelial cells. Nitric oxide is needed to maintain arterial relaxation (vasodilation). Impaired nitric oxide-dependent vasodilation is associated with increased risk of cardiovascular disease.

Decreasing platelet aggregation: Platelet aggregation is one of the first steps in the formation of a blood clot that can occlude a coronary or cerebral artery, resulting in myocardial infarction or stroke, respectively. Inhibiting platelet aggregation is considered an important strategy in the primary and secondary prevention of cardiovascular disease.

     
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