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Evidence-Based Complementary and Alternative Medicine
Volume 2013 (2013), Article ID 237207, 17 pages
http://dx.doi.org/10.1155/2013/237207
Research Article

Korean Red Ginseng Extract Attenuates 3-Nitropropionic Acid-Induced Huntington’s-Like Symptoms

1Department of Anatomy, College of Korean Medicine and Institute of Korean Medicine, Kyung Hee University, Seoul 130-701, Republic of Korea
2Department of Cancer Preventive Material Development and Institute of Korean Medicine, Kyung Hee University, Seoul 130-701, Republic of Korea
3Analysis Research Team, R&D Headquarters, Korea Ginseng Corporation, Daejeon 305-805, Republic of Korea

Received 15 September 2012; Revised 29 November 2012; Accepted 2 December 2012

Academic Editor: Bashar Saad

Copyright © 2013 Minhee Jang 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

Korean red ginseng (KRG) possesses neuroprotective activity. However, the potential neuroprotective value of KRG for the striatal toxicity is largely unknown. We investigated whether KRG extract (KRGE) could have a neuroprotective effect in a 3-nitropropionic acid- (3-NP) induced (i.p.) Huntington’s disease (HD) model. KRGE (50, 100, and 250 mg/kg/day, p.o.) was administrated 10 days before 3-NP injection (pre-administration), from the same time with 3-NP injection (co-administration), or from the peak point of neurological impairment by 3-NP injection (post-administration). Pre-administration of KRGE produced the greatest neuroprotective effect in this model. Pre-administration of KRGE significantly decreased 3-NP-induced neurological impairment, lethality, lesion area, and neuronal loss in the 3-NP-injected striatum. KRGE attenuated microglial activation and phosphorylation of mitogen-activated protein kinases (MAPKs) and nuclear factor-kappa B (NF-κB) signal pathway. KRGE also reduced the level of mRNA expression of tumor necrosis factor-alpha, interleukin- (IL-) 1β, IL-6, inducible nitric oxide synthase, and OX-42. Interestingly, the intrathecal administration of SB203580 (a p38 inhibitor) or PD98059 (an inhibitor of MAPK Kinase, MEK) increased the survival rate in the 3-NP-induced HD model. Pre-administration of KRGE may effectively inhibit 3-NP-induced striatal toxicity via the inhibition of the phosphorylation of MAPKs and NF-κB pathways, indicating its therapeutic potential for suppressing Huntington’s-like symptoms.