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Oxidative Medicine and Cellular Longevity
Volume 2016, Article ID 7124251, 9 pages
http://dx.doi.org/10.1155/2016/7124251
Research Article

Punicalagin Induces Serum Low-Density Lipoprotein Influx to Macrophages

1Department of Oxidative Stress and Human Diseases, MIGAL–Galilee Research Institute, 11016 Kiryat Shmona, Israel
2Tel-Hai College, 12208 Upper Galilee, Israel
3Faculty of Medicine in the Galilee, Bar-Ilan University, 1311502 Safed, Israel
4Eliachar Research Laboratory, Western Galilee Hospital, 22100 Nahariya, Israel

Received 24 January 2016; Revised 11 May 2016; Accepted 31 May 2016

Academic Editor: Gabriele Saretzki

Copyright © 2016 Dana Atrahimovich et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

High levels of circulating low-density lipoprotein (LDL) are a primary initiating event in the development of atherosclerosis. Recently, the antiatherogenic effect of polyphenols has been shown to be exerted via a mechanism unrelated to their antioxidant capacity and to stem from their interaction with specific intracellular or plasma proteins. In this study, we investigated the interaction of the main polyphenol in pomegranate, punicalagin, with apolipoprotein B-100 (ApoB100) that surrounds LDL. Punicalagin bound to ApoB100 at low concentrations (0.25–4 μM). Upon binding, it induced LDL influx to macrophages in a concentration-dependent manner, up to 2.5-fold. In contrast, another polyphenol which binds to ApoB100, glabridin, did not affect LDL influx. We further showed that LDL influx occurs specifically through the LDL receptor, with LDL then accumulating in the cell cytoplasm. Taken together with the findings of Aviram et al., 2000, that pomegranate juice and punicalagin induce plasma LDL removal and inhibit macrophage cholesterol synthesis and accumulation, our results suggest that, upon binding, punicalagin stimulates LDL influx to macrophages, thus reducing circulating cholesterol levels.