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The anti-atherosclerotic activity of vitamin E involves inhibition of oxidation of LDL and accumulation of oxLDL in the arterial wall. It also appears to reduce oxLDL-induced apoptosis in human endothelial cells. Oxidation of LDL is a critical early step in the formation of atherosclerosis because it triggers many events that lead to the formation of atherosclerotic plaque. In addition, vitamin E inhibits protein kinase C (PKC) activity. PKC plays a role in smooth muscle cell proliferation, and therefore, inhibition of PKC leads to inhibition of smooth muscle cell proliferation, which involves atherogenesis.
The antithrombotic and anticoagulant activity of vitamin E involves downregulating the expression of intracellular adhesion molecules (ICAM)-1 and vascular cell adhesion molecule (VCAM)-1, which reduces the adhesion of blood components to the endothelium. In addition, vitamin E upregulates the expression of cytosolic phospholipase A2 and cyclooxygenase (COX)-1, thereby enhancing the release of prostacyclin. Prostacyclin is an inhibitor of vasodilation factor and platelet aggregation and platelet release. It is also known that platelet aggregation is mediated by a mechanism involved in the binding of fibrinogen to platelet glycoprotein IIb / IIIa (GPIIb / IIIa) complex. GPIIb / IIIa is the major membrane receptor protein and is the key to platelet aggregation. GPIIb is the α-subunit of the platelet membrane protein. Alpha-tocopherol downregulates GPIIb promoter activity, resulting in decreased expression of GPIIb protein and decreased platelet aggregation. Vitamin E is also found in cultures to reduce plasma production of thrombin, a protein that binds to platelets and induces aggregation. The metabolite of vitamin E, called vitamin E or alpha-tocopherol (TQ), is an effective anticoagulant. This metabolite inhibits vitamin K-dependent carboxylase, which is the main enzyme in the coagulation cascade.
The neuroprotective effects of vitamin E can be explained by its antioxidant effects. Many neurological diseases are caused by oxidative stress. Vitamin E protects against the stress by protecting against the nervous system.
The immunomodulatory effects of vitamin E have been demonstrated in vitro, wherein alpha-tocopherol increases the mitogenic response of T lymphocytes from aged mice. The mechanism by which vitamin E responds to this reaction is unclear, but it is believed that vitamin E itself may have mitogenic activity unrelated to its antioxidant activity.
Finally, the mechanism of action of the antiviral effect of vitamin E (mainly against HIV-1) involves its antioxidant activity. Vitamin E reduces oxidative stress, which is thought to contribute to the pathogenesis of HIV-1, as well as the pathogenesis of other viral infections. Vitamin E also affects membrane integrity and fluidity, and since HIV-1 is a membrane virus, altering the membrane fluidity of HIV-1 may interfere with its ability to bind to cellular receptor sites, thereby reducing its infectivity.
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