Salicornia bigelovii Torr Attenuates Neuro-Inflammatory Responses in Lipopolysaccharide-Induced BV-2 Microglia by Regulation of NF-kappa B Signaling

Hyun Kang^1,2, Sushruta Koppula¹ and Tae-Kyu Park¹*

¹Department of Biotechnology, Research Institute for Biomedical & Health Science, College of Biomedical and Health Science, Konkuk University, ²KuGen Healthcare Institute, Konkuk University Business Incubation Center, Chungju, 380-701, Republic of Korea

*For correspondence: Email: taekyupark2@gmail.com; Tel: 82-43-840-3870; Fax: 82-43-852-3616

Received: 8 October 2013                                                                     Revised accepted: 7 November 2013

Tropical Journal of Pharmaceutical Research, December 2013; 12(6): 897-903

Purpose: To investigate the anti-oxidant and anti-neuroinflammatory effects of Salicornia bigelovii extract (SBE) in lipopolysaccharide (LPS)-stimulated BV-2 microglial cells.

Methods:  Anti-oxidant 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- diphenyl-tetrazolium bromide (MTT) assay. BV- microglial cells were stimulated with LPS to study the protein expression and production of inflammatory mediators, determined by Western blot analysis.

Results: SBE significantly inhibited the DPPH-generated free radicals showing maximum inhibition at 40 µg/mL (p < 0.001). SBE alone did not exhibit any signs of cytotoxicity to BV-2 cells up to 200 µg/mL concentration. The LPS-induced increase in the production of nitric oxide was concentration-dependently suppressed by SBE (p < 0.05 for 10 µg/mL, p < 0.01 at 20 µg/mL and p < 0.001 at 40 µg/mL, respectively). SBE also inhibited the LPS-induced increase in inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) expressions. Further, the production of proinflammatory cytokines such as tumor necrosis factor-α and interleukin-6 by LPS-stimulation in BV-2 cells was inhibited by SBE pretreatment. Mechanistic study revealed that SBE acts by regulation of nuclear factor kappa-B signaling pathway in LPS-stimulated BV-2 microglial cells.

Conclusion: This study revealed for the first time that SBE possesses anti-oxidant and anti-neuroinflammatory effects and can be developed as a potential therapeutic target in ameliorating microglia-mediated neuroinflammation.