Tropical Journal of Pharmaceutical Research

Original Research Article | OPEN ACCESS

Inhibition of Lipopolysaccharide-Induced Neuroinflammatory Events in Bv-2 Microglia by Chestnut Peel Extract

Hyun Kang

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

For correspondence:- Email: hyunbio@gmail.com Tel:+82415501481

Received: 14 July 2013 Accepted: 6 September 2014 Published: 19 October 2014

Citation: Kang H. Inhibition of Lipopolysaccharide-Induced Neuroinflammatory Events in Bv-2 Microglia by Chestnut Peel Extract. Trop J Pharm Res 2014; 13(10):1615-1620 doi: 10.4314/tjpr.v13i10.7

© 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 evaluate the protective effects of chestnut (Castenea cranata Siebold & Zucc., Fagaceae) peel extract on stimulated BV-2 microglial cells as well as its anti-oxidant properties.

Methods: The ethyl acetate fraction of C.cranata peel (CCP) extract was used in the study to evaluate the anti-neuroinflammatory effects in BV-2 microglial cells. Cell viability was performed by 3-(4, 5-dimethylthiazol-2-yl)-2, 5- diphenyl-tetrazolium bromide (MTT) assay. Lipopolysaccharide (LPS) is used to activate BV-2 microglia. Nitric oxide (NO) levels were measured using Griess assay. Inducible NO synthase (iNOS) expressional levels were measured by Western blot analysis. Tumor necrosis factor-alpha (TNF-α) production was evaluated by enzyme-linked immunosorbent assay (ELISA). Anti-oxidant properties were evaluated by 1, 1-diphenyl-2-picryl-hydrazyl (DPPH) radical scavenging assay.

Results: LPS-activated excessive release of NO in BV-2 cells was significantly inhibited (p < 0.001 at 100 μg/mL) by CCP extract. LPS-induced excessive production of inflammatory mediator such as iNOS was also significantly attenuated by CCP extract. Further, CCP extract significantly and dose dependently inhibited the TNF-α levels in LPS-induced BV-2 microglial cells (p < 0.05 at 20 μg/mL, p < 0.01 at 40 μg/mL and p < 0.001 at 80 and 100 μg/mL). CCP extract also scavenged DPPH radicals in a dose-dependent fashion (p < 0.05 at 0.01 mg/mL and p < 0.001 at 0.1 and 1 mg/mL) with an IC50 value of 0.08 μg/mL.

Conclusion: Data from this study indicate that CCP extract attenuates neuroinflammatory responses in LPS-activated BV-2 microglia by inhibiting excessive production of pro-inflammatory mediators such as NO, iNOS and TNF-α. The strong anti-oxidant effect of CCP extract suggests that it possesses anti-neuroinflammatory properties.

Keywords: Castenea cranata, Chestnut peel extract, DPPH radicals, Anti-oxidant, Neuroinflammation, BV-2 microglia