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Original Research Article | OPEN ACCESS

Aralia elata (Miquel) Seemann suppresses inflammatory responses in macrophage cell by regulation of NF-kappa B signalling

Chong-Heon Lee1, Hyun Kang2

1Department of Oral Pathology, College of Dentistry; 1Department of Oral Pathology, College of Dentistry; 2Department of Medical Laboratory Science, College of Health Sciences, Dankook University, Cheonan-si, Chungnam, 330-714, Republic of Korea;

For correspondence:-  Hyun Kang   Email: hyunbio@gmail.com, hkang@dankook.ac.kr   Tel:+82415501452

Received: 5 January 2015        Accepted: 28 February 2015        Published: 31 March 2015

Citation: Lee C, Kang H. Aralia elata (Miquel) Seemann suppresses inflammatory responses in macrophage cell by regulation of NF-kappa B signalling. Trop J Pharm Res 2015; 14(3):423-429 doi: 10.4314/tjpr.v14i3.10

© 2015 The authors.
This is an Open Access article that uses a funding model which does not charge readers or their institutions for access and distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0) and the Budapest Open Access Initiative (http://www.budapestopenaccessinitiative.org/read), which permit unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited..

Abstract

Purpose: To investigate the antioxidant and anti-inflammatory effects of Aralia elata extract (AEE) in lipopolysaccharide (LPS)-stimulated Raw264.7 cells.
Methods: Antioxidant activity was measured using 1, 1-diphenyl-2-picryl-hydrazyl (DPPH) radical scavenging assay. Cell viability was evaluated using 3-(4, 5-dimethylthiazol-2-yl)-2, 5- diphenyltetrazolium bromide (MTT) assay. RAW264.7 cells were stimulated with LPS to study protein expression and production of inflammatory mediators, determined by Western blot analysis.
Results: AEE significantly inhibited DPPH-generated free radicals showing maximum inhibition at 40 μg/mL (p < 0.001). AEE alone did not exhibit any signs of cytotoxicity to RAW264.7 cells up to 200 μg/mL concentration. The LPS-induced increase in the production of nitric oxide was concentration-dependently suppressed with half-maximal concentration (IC50) of 91.5 ug/ mL of AEE (p < 0.05 at 10 μg/mL, p < 0.01 at 20 μg/mL and p < 0.001 at 40 μg/mL, respectively). AEE also inhibited dose-dependently the LPS-induced increase in inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) expressions with IC50 of 72.5 ug/ mL. Furthermore, the production of pro-inflammatory cytokines, viz, tumor necrosis factor-α by LPS-stimulation in RAW264.7 cells was inhibited dose-dependently with IC50 of 34.9 ug/ mL by AEE pretreatment. Mechanistic studies revealed that AEE acts by regulation of nuclear factor kappa-B signaling pathway in LPS-stimulated RAW264.7 cells.
Conclusion: This study shows, for the first time, that AEE possesses antioxidant and anti-inflammatory effects and can be developed as a potential therapeutic agent for ameliorating macrophage-mediated inflammation.

Keywords: Aralia elata, Anti-inflammatory activity, Macrophage cells, Inducible nitric oxide synthase, nuclear factor kappa-B signaling

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Thompson Reuters (ISI): 0.523 (2021)
H-5 index (Google Scholar): 39 (2021)

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