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Mediators of Inflammation
Volume 2012, Article ID 732860, 7 pages
http://dx.doi.org/10.1155/2012/732860
Research Article

Molecular Mechanism of Macrophage Activation by Red Ginseng Acidic Polysaccharide from Korean Red Ginseng

1Department of Genetic Engineering, Sungkyunkwan University, Suwon 440-746, Republic of Korea
2College of Pharmacy, Chung-Ang University, Seoul 122-704, Republic of Korea
3Korea Ginseng Corporation, Central Research Institute, Daejeon 305-805, Republic of Korea
4Department of Efficacy Screening, Hongcheon Institute of Medicinal Herb, Hongcheon 250-930, Republic of Korea
5Department of Natural Product Resources, DanjoungBio, Wonju 220-842, Republic of Korea
6College of Veterinary Medicine, Kyungpook National University, Daegu 702-701, Republic of Korea

Received 10 August 2011; Accepted 1 October 2011

Academic Editor: Antonio Macciò

Copyright © 2012 Se Eun Byeon 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

Red ginseng acidic polysaccharide (RGAP), isolated from Korean red ginseng, displays immunostimulatory and antitumor activities. Even though numerous studies have been reported, the mechanism as to how RGAP is able to stimulate the immune response is not clear. In this study, we aimed to explore the mechanism of molecular activation of RGAP in macrophages. RGAP treatment strongly induced NO production in RAW264.7 cells without altering morphological changes, although the activity was not strong compared to LPS-induced dendritic-like morphology in RAW264.7 cells. RGAP-induced NO production was accompanied with enhanced mRNA levels of iNOS and increases in nuclear transcription factors such as NF-κB, AP-1, STAT-1, ATF-2, and CREB. According to pharmacological evaluation with specific enzyme inhibitors, Western blot analysis of intracellular signaling proteins and inhibitory pattern using blocking antibodies, ERK, and JNK were found to be the most important signaling enzymes compared to LPS signaling cascade. Further, TLR2 seems to be a target surface receptor of RGAP. Lastly, macrophages isolated from RGS2 knockout mice or wortmannin exposure strongly upregulated RGAP-treated NO production. Therefore, our results suggest that RGAP can activate macrophage function through activation of transcription factors such as NF-κB and AP-1 and their upstream signaling enzymes such as ERK and JNK.