Many natural products, including vitamin E, garlic, purpurogallin, flaxseed and its components [secoisolariciresinol diglucoside (SDG) and flax lignan complex (FLC)] and resveratrol have been reported to suppress hypercholesterolemic atherosclerosis. It is known that all of the drugs that suppress the development of atherosclerosis do not regress and/or slow the progression of atherosclerosis. To be of potential benefit in patients with established atherosclerosis, a drug should produce regression and/or slow the progression of atherosclerosis. In this review, the effects of vitamin E, SDG and FLC in the regression and slowing of progression of hypercholesterolemic atherosclerosis and their mechanisms have been described. The effectiveness of vitamin E in patients with established coronary disease is very controversial. However, in experimental animal controlled studies, vitamin E does not regress or slow the progression of hypercholesterolemic atherosclerosis. The mechanisms of the ineffectiveness of vitamin E in regression and slowing of progression of atherosclerosis have been discussed. SDG is effective in slowing the progression of atherosclerosis and partially effective in regression of hypercholesterolemic atherosclerosis. These effects are associated with reduction in oxidative stress. FLC does not regress hypercholesterolemic atherosclerosis but slows the progression of hypercholesterolemic atherosclerosis. Slowing of progression is associated with reduction on oxidative stress. In conclusion, vitamin E does not regress or slow the progression of established atherosclerosis. SDG slows the progression and regresses established atherosclerosis. FLC does not regress but slows the progression of established atherosclerosis.
Flax lignan complex, oxidative stress, progression of atherosclerosis, regression of atherosclerosis, secoisolariciresinol diglucoside, serum lipids, vitamin E, purpurogallin, flaxseed, secoisolariciresinol diglucoside (SDG), atherosclerosis, coronary disease, Purpurogallin, probucol, antioxidant, hypolipidemic agent, xanthomas, nifedipine, verapamil, angiotensin-converting enzyme (ACE), perindopril, Captopril, atorvastatin, Lovastatin, Reactive oxygen species (ROS), glutathione peroxidase, apolipoprotein, low-density lipoprotein (LDL), myocardial infarction, aortic chemiluminescent activity, tocopherol, fluvastatin, cinnamic acid, Hydroxymethylglutaric acid, angiotensin-converting enzyme inhibitors, guanosine monophosphate (GMP)
Department of Physiology, College of Medicine, University of Saskatchewan, 107 Wiggins Road, Saskatoon, SK, S7N 5E5, Canada.