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Enhancement of Type A Macrophage Scavenger Receptor Expression by Ginsenoside Rg3 in Rat Microglia  

Joo, Seong-Soo (College of Pharmacy, Chung-Ang University)
Hwang, Kwang-Woo (College of Pharmacy, Chung-Ang University)
Lee, Do-Ik (College of Pharmacy, Chung-Ang University)
Publication Information
YAKHAK HOEJI / v.49, no.2, 2005 , pp. 147-150 More about this Journal
Abstract
Macrophage scavenger receptors (MSRs) induce microglial interaction with ${\beta}$-amyloid fibrils (fA${\beta}$) that are associated with Alzheimer's disease (AD). Although microglia are know n to have a dual effect on formation of plaque and clearance of fA${\beta}$ in the AD brain, receptor-mediated phagocytosis is a very important tool for preventing amyloid plaque via activated microglia in the early stage of AD. In the study, we examined whether ginsonoside Rg3 enhances the microglial Phagocytosis of A${\beta}$1-42 through Phagocytosis assay, gene expression (RT-PCR) and protein assay (western blots) for the cell responsiveness presented between Rg3-treated and non-treated groups. Fluro-labeled Ac-LDL and E.coli particles were used as control proteins for phagocytosis. In previous studies, this was a particularly interesting property of Rg3 in the stimulation and phagocytosis of macrophages in the periphery. We report here that ginsenoside Rg3 increased the expression of type-A MSR (MSR-A) in microglia and thus accelerated the phagocytosis with an effective degradation of engulfed fA${\beta}$. This result suggests that Rg3 may play an important role in removing fA${\beta}$ by enhancing the receptor-mediated phagocytosis. In addition, Rg3 could be a potential candidate for balancing the rate of production of fA${\beta}$ in AD brain.
Keywords
${\beta}$-amyloid; MSR-A; Alzheimer's disease; ginsenoside Rg3; microglia;
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