Article Sidebar
Published:
Jan 20, 2014DOI:
10.4314/tjpr.v12i6.6Keywords:
Article Details
Submission of a manuscript to this journal is a representation that the manuscript has not been published previously and is not under consideration for publication elsewhere.
All authors named in each manuscript would be required to sign a form (to be supplied by the Editor) so that they may retain their copyright in the article but to assign to us (the Publishers) and its licensees in perpetuity, in all forms, formats and media (whether known or created in the future) to (i) publish, reproduce, distribute, display and store the contribution, (ii) translate the contribution into other languages, create adaptations, reprints, include within collections and create summaries, extracts and/or abstracts of the contribution, (iii) create any other derivative works(s) based on the contribution, (iv) to exploit all subsidiary rights in the contribution, (v) the inclusion of electronic links from the contribution to third party material where-ever it may be located, and (vi) license any thrid party to do any or all of the above.
Main Article Content
Salicornia bigelovii Torr Attenuates Neuro-Inflammatory Responses in Lipopolysaccharide-Induced BV-2 Microglia by Regulation of NF-kappa B Signaling
Abstract
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- diphenyltetrazolium 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 concentrationdependently 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 antineuroinflammatory effects and can be developed as a potential therapeutic target in ameliorating microglia-mediated neuroinflammation.
Keywords: Salicornia bigelovii, Anti-oxidant, lipopolysaccharide; Neuroinflammation, Microglia, Cyclooxygenase, iNOS, NF-κB.
