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

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, 5diphenyltetrazolium bromide (MTT) assay. BVmicroglial 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.