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Original Research Article | OPEN ACCESS

Inhibition of Lipopolysaccharide-Stimulated Neuro-Inflammatory Kuntze in BV-2 Microglial Cell Mediators by Tetragonia tetragonoides (Pall)

Sung-Gyu Lee, Hyun Kang ,

Department of Medical Laboratory Science, College of Health Science, Dankook University, Cheonan-si, Chungnam, 330-714, Republic of Korea;

For correspondence:-  Hyun Kang   Email: hkang@dankook.ac.kr   Tel:082-41-550-1452

Received: 29 September 2014        Accepted: 12 November 2014        Published: 15 December 2014

Citation: Lee S, Kang H, Inhibition of Lipopolysaccharide-Stimulated Neuro-Inflammatory Kuntze in BV-2 Microglial Cell Mediators by Tetragonia tetragonoides (Pall). Trop J Pharm Res 2014; 13(12):2005-2010 doi: 10.4314/tjpr.v13i12.8

© 2014 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 in vitro antioxidant and anti-neuroinflammatory effects of Tetragonia tetragonoides (Pall.) Kuntze extract (TKE) in lipopolysaccharide (LPS)-stimulated BV-2 microglial cells.
Methods:  To evaluate the effects of TKE, LPS-stimulated BV microglia were used and the expression and production of inflammatory mediators, namely, nitric oxide (NO), inducible NO synthase (iNOS) and tumor necrosis alpha (TNF-α) were evaluated. Antioxidant activity of TKE was measured using 1, 1-diphenyl-2-picryl-hydrazyl (DPPH) assay. Cell viabilities were estimated by 3-(4, 5-dimethylthiazol-2-yl)-2, 5- diphenyl-tetrazolium bromide (MTT) assay.
Results:TKE significantly suppressed LPS-induced production of NO (p < 0.001 at 20, 40, 80 and 100 μg/ml) and expression of iNOS in BV-2 cells. TKE also suppressed LPS-induced increase in TNF-α level (p < 0.001at 100 μg/ml) in BV-2 cells. In addition, DPPH-generated free radicals were inhibited by TKE in a concentration-dependent manner.
Conclusion:The results suggest that TKE can be explored as a potential therapeutic agent for regulating microglia-mediated neuroinflammatory responses observed in several neurodegenerative diseases.

Keywords: Tetragonia tetragonoides, Anti-oxidant, Anti-inflammatory, Neurodegenerative diseases, Microglial cells, Lipopolysaccharide

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

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