Carnosine and its constituents inhibit glycation of low-density lipoproteins that promotes foam cell formation in vitro
Abstract
Glycation of low-density lipoprotein (LDL) by reactive aldehydes, such as glycolaldehyde, can result in the cellular accumulation of cholesterol in macrophages. In this study, it is shown that carnosine, or its constituent amino acids β-alanine and l-histidine, can inhibit the modification of LDL by glycolaldehyde when present at equimolar concentrations to the modifying agent. This protective effect was accompanied by inhibition of cholesterol and cholesteryl ester accumulation in human monocyte-derived macrophages incubated with the glycated LDL. Thus, carnosine and its constituent amino acids may have therapeutic potential in preventing diabetes-induced atherosclerosis.
Abbreviations: AGE, advanced glycation end products, β-Ala, β-alanine, CN, carnosine, GA, glycolaldehyde, His, histidine, HMDM, human monocyte-derived macrophages, REM, relative electrophoretic mobility
Keywords: Atherosclerosis, Aldehyde, Carnosine, Foam cell, Glycation, Low-density lipoprotein
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PII: S0014-5793(07)00130-5
doi:10.1016/j.febslet.2007.01.082
© 2007 Federation of European Biochemical Societies
