Potential effects of microglial activation induced by ginsenoside Rg3 in rat primary culture: Enhancement of type a macrophage scavenger receptor expression
Brain microglia are phagocytic cells that are the major inflammatory response cells of the central nervous system and widely held to play important pathophysiologic roles in Alzheimer's disease (AD) in both potentially neurotoxic responses and potentially beneficial phagocytic responses. In the...
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Published in | Archives of pharmacal research Vol. 28; no. 10; pp. 1164 - 1169 |
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Main Authors | , |
Format | Journal Article |
Language | English |
Published |
Korea (South)
Pharmaceutical Society of Korea
01.10.2005
대한약학회 |
Subjects | |
Online Access | Get full text |
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Summary: | Brain microglia are phagocytic cells that are the major inflammatory response cells of the central nervous system and widely held to play important pathophysiologic roles in Alzheimer's disease (AD) in both potentially neurotoxic responses and potentially beneficial phagocytic responses. In the study, we examined whether ginsonoside Rg3, a by-product of red ginseng, enhances the microglial phagocytosis of Aβ. We found that Rg3 promoted Aβ uptake, internalization, and digestion. Increased maximal Aβ uptake was observed at 4 and 8 h after Rg3 pretreatment (25 μg/mL), and the internalized Aβ was almost completely digested from cells within 36 h when pretreated with Rg3 comparing with single non-Rg3-treated groups. The expression of MSRA (type A MSR) was also up-regulated by Rg3 treatment in a dose-and time-dependent manner which was coincidently identified in western blots for MSRA proteins in cytosol. These results indicate that microglial phagocytosis of Aβ may be enhanced by Rg3 and the effect of Rg3 on promoting clearance of Aβ may be related to the MSRA-associated action of Rg3. Thus, stimulation of the MSRA might contribute to the therapeutic potentials of Rg3 in microglial phagocytosis and digestion in the treatment of AD. |
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Bibliography: | http://dx.doi.org/10.1007/BF02972981 G704-000010.2005.28.10.010 |
ISSN: | 0253-6269 1976-3786 |
DOI: | 10.1007/bf02972981 |