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Evidence-Based Complementary and Alternative Medicine
Volume 2014 (2014), Article ID 837835, 11 pages
Research Article

Beneficial Effects of Fractions of Nardostachys jatamansi on Lipopolysaccharide-Induced Inflammatory Response

1Hanbang Body-Fluid Research Center, Wonkwang University, Iksan, Jeonbuk 540-749, Republic of Korea
2Department of Rehabilitation Medicine of Korean Medicine, Spine & Joint Center, Pusan National University Korean Medicine Hospital, Yangsan 626-770, Republic of Korea
3Department of Herbology, School of Oriental Medicine, Wonkwang University, Iksan, Jeonbuk 540-749, Republic of Korea
4BK21 plus team, Professional Graduate School of Oriental Medicine, Wonkwang University, Iksan, Jeonbuk 540-749, Republic of Korea
5Department of Beauty, Dongshin University, Naju, Jeonnam 252-17, Republic of Korea
6College of Pharmacy, Wonkwang University, Iksan 570-749, Republic of Korea

Received 19 November 2013; Revised 28 February 2014; Accepted 3 March 2014; Published 30 March 2014

Academic Editor: MinKyun Na

Copyright © 2014 Gi-Sang Bae 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.


It has been previously shown that Nardostachys jatamansi (NJ) exhibits anti-inflammatory properties against lipopolysaccharide (LPS) challenges. However, the potency of NJ constituents against LPS-induced inflammatory responses has not been examined. In this present study, we determined which NJ extract fractions exhibit inhibitory effects against LPS-induced inflammatory responses. Among the NJ fractions, NJ-1, NJ-3, NJ-4, and NJ-6 inhibited LPS-induced production of NO. The NJ-3, NJ-4, and NJ-6 fractions also inhibited the production of cytokines, such as IL-1β, IL-6, and TNF-α. However, NJ-1, NJ-3, NJ-4, and NJ-6 showed differential inhibitory mechanisms against LPS-induced inflammatory responses. NJ-1, NJ-3, and NJ-4 inhibited LPS-induced activation of c-jun NH2-terminal kinase (JNK) and p38 but did not affect activation of extracellular signal-regulated kinase (ERK) or NF-κB. On the other hand, NJ-6 inhibited activation of MAPKs and NF-κB. In addition, in vivo experiments revealed that administration of NJ-1, NJ-3, NJ-4, and NJ-6 reduced LPS-induced endotoxin shock, with NJ-6 especially showing a marked protective effect. Taken together, these results provide the evidence for the potential of selective NJ fractions against LPS-induced inflammation. Thus, it will be advantageous to further isolate and determine single effective compounds from these potent fractions.