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Vitamin E reduces progression of atherosclerosis in low-density lipoprotein receptor-deficient mice with established

Tillmann Cyrus1, Yuemang Yao, Joshua Rokach

  • 1Center for Experimental Therapeutics and Department of Pharmacology, University of Pennsylvania, School of Medicine, Philadelphia, Pa 19104, USA.

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Vitamin E supplementation in mice with established atherosclerosis reduced disease progression by lowering oxidative stress and inflammation. This study highlights vitamin E

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Area of Science:

  • Cardiovascular Research
  • Nutritional Science
  • Biomedical Research

Background:

  • Oxidative stress is implicated in early atherogenesis, but clinical trials with antioxidant vitamins in humans with established atherosclerosis yield inconsistent results.
  • Animal studies suggest a significant role for oxidative stress-mediated mechanisms in the development of atherosclerosis.

Purpose of the Study:

  • To investigate the effect of vitamin E supplementation on established atherosclerosis in a mouse model.
  • To determine if vitamin E can mitigate oxidative stress and inflammatory responses associated with atherosclerosis progression.

Main Methods:

  • Low-density lipoprotein receptor-deficient (LDLR KO) mice were fed a high-fat diet to induce atherosclerosis.
  • Mice with established atheroma were randomized to receive a high-fat diet with or without vitamin E supplementation for 3 months.
  • Biomarkers of oxidative stress, inflammation, and nitric oxide levels were measured.

Main Results:

  • Vitamin E supplementation significantly reduced 8,12-iso-isoprostane (iP)F(2alpha)-VI and monocyte chemoattractant protein-1 levels.
  • Nitric oxide levels were increased in vitamin E-treated mice compared to placebo.
  • While the placebo group showed atherosclerosis progression, vitamin E-treated animals exhibited a significant reduction in disease progression.
  • No significant differences in lipid levels were observed between the groups.

Conclusions:

  • Vitamin E supplementation effectively reduces the progression of established atherosclerosis in LDLR KO mice.
  • The mechanism involves suppressing oxidative and inflammatory reactions and enhancing nitric oxide bioavailability.
  • These findings suggest a potential therapeutic role for vitamin E in managing atherosclerosis.