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Evidence-Based Complementary and Alternative Medicine
Volume 2015, Article ID 768049, 10 pages
http://dx.doi.org/10.1155/2015/768049
Research Article

PMC-12, a Prescription of Traditional Korean Medicine, Improves Amyloid -Induced Cognitive Deficits through Modulation of Neuroinflammation

1Division of Meridian and Structural Medicine, School of Korean Medicine, Pusan National University, Yangsan, Gyeongnam 626-870, Republic of Korea
2Korean Medical Science Research Center for Healthy Aging, Pusan National University, Yangsan, Gyeongnam 626-870, Republic of Korea
3Department of Horticultural Bioscience, College of Natural Resource and Life Science, Pusan National University, Miryang, Gyeongnam 626-706, Republic of Korea
4Department of Pharmacy, College of Pharmacy, Pusan National University, Busan 609-735, Republic of Korea
5Research Center for Anti-Aging Technology Development, Pusan National University, Busan 609-735, Republic of Korea
6Division of Humanities and Social Medicine, School of Korean Medicine, Pusan National University, Yangsan, Gyeongnam 626-870, Republic of Korea

Received 18 February 2015; Revised 28 March 2015; Accepted 28 March 2015

Academic Editor: Ki-Wan Oh

Copyright © 2015 Min Young Park 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

PMC-12 is a prescription used in traditional Korean medicine that consists of a mixture of four herbal medicines, Polygonum multiflorum, Rehmannia glutinosa, Polygala tenuifolia, and Acorus gramineus, which have been reported to have various pharmacological effects on age-related neurological diseases. In the present study, we investigated whether PMC-12 improves cognitive deficits associated with decreased neuroinflammation in an amyloid-β-(Aβ-) induced mouse model and exerts the antineuroinflammatory effects in lipopolysaccharide-(LPS-) stimulated murine BV2 microglia. Intracerebroventricular injection of in mice resulted in impairment in learning and spatial memory, whereas this was reversed by oral administration of PMC-12 (100 and 500 mg/kg/day) in dose-dependent manners. Moreover, PMC-12 reduced the increase of Aβ expression and activation of microglia and astrocytes in the -injected brain. Furthermore, quantitative PCR data showed that inflammatory mediators were significantly decreased by administration of PMC-12 in Aβ-injected brains. Consistent with the in vivo data, PMC-12 significantly reduced the inflammatory mediators in LPS-stimulated BV2 cells without cell toxicity. Moreover, PMC-12 exhibited anti-inflammatory properties via downregulation of ERK, JNK, and p38 MAPK pathways. These findings suggest that the protective effects of PMC-12 may be mediated by its antineuroinflammatory activities, resulting in the attenuation of memory impairment; accordingly, PMC-12 may be useful in the prevention and treatment of AD.