| Background: Several epidemiological studies have demonstrated that plasma levels of HDL and apo A-I are inversely correlated with the incidence of coronary heart disease. These observations suggest that HDL may play a protective role in atherogenesis. The antiatherogenic properties of HDL or apoA-1 have also been demonstrated in experimental animals. Transgenic mice overexpression human apo A-I are much more resistant to diet-induced atherosclerosis than nontransgenic mice. The most important characteristic of atherosclerotic arteries is the accumulation of cholesterol within the vessel wall as a consequence of an unbalanced influx-efflux. Reverse cholesterol transport seems to be the major route for removal of the exchangeable cholesterol deposited in tissues that do not metabolize it, and for its transport to the liver and subsequent metabolization. The concept of a reverse cholesterol transport pathway, with the HDL particle serving as scavenger of tissue cholesterol, has been enthusiastically accepted since it was postulated. The role of plasma HDL as the preferential physiological acceptor for cholesterol from extrahepatic cells in vivo has been strongly supported by epidemiologic and in vitro studies. Furthermore, Badimon and his colleagues have reported that homologous HDL plasma fraction inhibits the development of fatty streaks and lipid deposition in the aortic wall of cholesterol-fed rabbits. However, reported results about the role of HDL in preventive and/or therapeutic treatment to rabbits do not showthe plasma lipid modulation of HDL in cholesterol-fed rabbits. The aim of present study was to determine whether human HDL could affect the progression and/or regression of established atherosclerotic lesions in the cholesterol-fed rabbits. Furthermore, we also examined the comparable effects of HDL with lovastatin on the atherosclerotic lesion formation and plasma lipid affection. The present study sought to determine if human high density lipoprotein injection administration could inhibit atherosclerosis lesions or reverse its further development.Atherosclerosis is one of the main complications of diabetes. In diabetes mellitus, HDL levels are usually decreased. Several factors may be involved, such as a decrease in triglyceride-rich lipoprotein catabolism and accelerated plasma clearance of HDL. Hyperglycemia in diabetic patients results in non-enzymatic glycation of plasma proteins, including lipoproteins such as high density lipoprotein (HDL). It is not clearly known whether there is increased oxidation of HDL in individuals with diabetes. We determined the effects of in vitro glycation of HDL on the susceptibility of HDL to oxidation and its capacity to mediate cholesterol efflux from macrophages. The effects of combined glycation and oxidation on the capacity of HDL-mediated cellular cholesterol efflux was also determined.The level of high density lipoprotein (HDL) in plasma is an equally strong or stronger inverse predictor of atheroscelerotic vascular disease risk than LDL. The decrease in atherosclerosis associated with increased HDL levels in humanapolipoprotein A-I (apo AI) transgenic animals further illustrates the protective nature of HDL. As with the LDL, oxidative modification that would affect the capacity of HDL to protect against atherosclerosis are of considerable importance and interest. The exact beneficial effects of HDL in vivo remain unknown. In vitro evidence suggests several potential protective actions. The best described of these is the ability of HDL to promotes the removal of excess cholesterol from peripheral cells, the first step in a pathway referred to as "reverse cholesterol transport". The initial removal of peripheral cell cholesterol by HDL particles is likely the rate-limiting step of this pathway. In addition, the removal of peripheral cell lipids by nascent HDL appears to be a key determinant of circulating HDL cholesterol levels.HDL may also be protective by inhibiting the oxidation of LDL, and by neutralizing the atherogenic effects...
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