Carum carvi Linn (Umbelliferae) Attenuates Lipopolysaccharide-Induced Neuroinflammatory Responses via Regulation of NF-κB Signaling in BV-2 Microglia
Abstract
Purpose: To investigate the anti-neuroinflammatory properties of Carum carvi Linn. (CCE, Umbelliferae) aqueous extract in stimulated BV-2 microglial cells and explore its underlying mechanisms.
Methods: Cell viability assessment was performed by 3-(4, 5-dimethylthiazol-2-yl)-2, 5- diphenyltetrazolium bromide (MTT) assay. Lipopolysaccharide (LPS) was used to activate BV-2 microglia. Nitric oxide (NO) levels were measured using Griess assay. Inducible NO synthase (iNOS) and cyclooxygenase (COX) levels were evaluated by Western blot analysis. Interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α) production were evaluated by enzyme-linked immunosorbent assay (ELISA).
Results: CCE alone did not exhibit any signs of cytotoxicity to BV-2 cells up to 200 μg/ml concentration. The LPS-activated excessive release of NO in BV-2 cells was significantly inhibited by CCE (p < 0.001 at 100 μg/mL). CCE also inhibited the production of inflammatory mediators such as iNOS, COX-2, IL-6 and TNF-α (p < 0.05, p < 0.01 and p < 0.001 at 25, 50 and 100 μg/mL, respectively). Further mechanistic study revealed that CCE acts by regulation of nuclear factor kappa-B (NF-κB) signaling pathway in LPS-stimulated BV-2 microglial cells.
Conclusion: The results reveal that CCE exhibited its anti-neuroinflammatory effects via regulation of NF-κB signaling. This can be developed as a potential therapeutic target in ameliorating microgliamediated neuroinflammation.
Keywords: Carum carvi, Anti-oxidant, Neuroinflammation, Microglia, Nitric oxide, Interleukin
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.
