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Published on: July 21, 2012
The effect of alpha-tocopherol on monocyte proatherogenic activity
1Department of Pathology, University of Texas Southwestern Medical Center, Dallas, TX 75390-9073, USA. jialal.i@pathology.swmed.edu
Insights
Alpha-tocopherol (AT), a form of vitamin E, reduces oxidative stress and inflammation. AT supplementation benefits cardiovascular health by improving monocyte function and inhibiting key pathways in atherosclerosis development.
Area of Science:
- Cardiovascular Science
- Immunology
- Nutritional Science
Background:
- Atherosclerosis is a primary cause of death in Western countries.
- Monocytes play a critical role throughout all stages of atherosclerotic lesion development.
- alpha-Tocopherol (AT) is a potent lipid-soluble antioxidant and the primary form of vitamin E.
Purpose of the Study:
- To investigate the effects of alpha-tocopherol (AT) supplementation on monocyte function in relation to atherosclerosis.
- To elucidate the mechanisms by which AT influences monocyte-mediated inflammatory and adhesion processes.
Main Methods:
- Monocyte function was assessed following AT supplementation (1200 IU/d).
- Evaluated the release of reactive oxygen species, lipid oxidation, and cytokines (IL-1β, TNF-α).
- Examined monocyte adhesion to endothelium and the expression of adhesion molecules (CD11b, VLA-4), and NF-κB activity.
Main Results:
- AT supplementation decreased reactive oxygen species and lipid oxidation in monocytes.
- Reduced the release of pro-inflammatory cytokines, including IL-1β and TNF-α.
- Inhibited monocyte adhesion to endothelium by downregulating CD11b, VLA-4, and NF-κB activation.
Conclusions:
- AT exhibits anti-inflammatory and antiatherogenic properties by modulating monocyte function.
- AT supplementation reduces oxidative stress, cytokine release, and monocyte adhesion, crucial factors in atherogenesis.
- These findings highlight the therapeutic potential of AT in preventing and managing atherosclerosis.
Abstract:
Atherosclerosis is the leading cause of morbidity and mortality in Westernized populations. The monocyte is a crucial cell in the genesis of the atherosclerotic lesion and is present during all stages of atherosclerosis. alpha-Tocopherol (AT) is the most active component of the vitamin E family and is the principal and most potent lipid-soluble antioxidant in plasma and LDL. With regard to monocyte function, AT supplementation (1200 IU/d) has been shown to decrease release of reactive oxygen species, lipid oxidation, release of cytokines such as interleukin-1ss (IL-1ss) and tumor necrosis factor-alpha (TNF-alpha) and decrease adhesion of monocytes to human endothelium. The mechanism of inhibition of superoxide and lipid oxidation by monocytes appears to be via inhibition of protein kinase C (PKC), the decrease in IL-1ss and TNF-alpha release by inhibition of 5-lipoxygenase and the inhibition of monocyte-endothelial cell adhesion via decrease in adhesion molecules on monocytes, CD11b and VLA-4 and by decreasing DNA-binding activity of nuclear transcription factor kappaB. Thus, in addition to the decrease in oxidative stress resulting from AT supplementation, as evidenced by decreased F(2)-isoprostanes and LDL oxidizability, AT is anti-inflammatory and exerts beneficial antiatherogenic effects on cells crucial in atherogenesis such as monocytes.
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