Methanol Extract of Hydroclathrus clathratus Inhibits Production of Nitric Oxide, Prostaglandin E2 and Tumor Necrosis Factor-α in Lipopolysaccharidestimulated BV2 Microglial Cells via Inhibition of NF-κB Activity
Abstract
Purpose: Hydroclathrus clathratus is a brown marine seaweed known to possess anti-cancer, anti-herpetic, and anti-coagulant activities. The present study is aimed at investigating some anti-inflammatory effects of H. clathratus.
Methods: We investigated the anti-inflammatory effects of the methanol extract of H. clathratus (MEHC) by expression of mRNA and protein using RT-PCR and Western blot analysis in lipopolysaccharide (LPS)-stimulated BV2 microglial cells. The level of nitric oxide (NO) production was analyzed using Griess reaction. The release of prostaglandin E2 (PGE2) and tumor necrosis factor-α (TNF-α) were determined using sandwich ELISA. NF-κB activation was detected using EMSA methods.
Results: The results obtained indicate that the extract (MEHC) inhibited LPS-induced NO, PGE2, and TNF-α production without any significant cytotoxicity (p < 0.05). MEHC also inhibited production of inducible NO synthase (iNOS), cyclooxygenase-2 (COX-2) and TNF-α mRNA in LPS-stimulated BV2 microglial cells. In addition, MEHC significantly reduced (p < 0.05) nuclear translocation of the nuclear factor-κB (NF-κB) subunits, p50 and p65, and its DNA-binding activity in LPS-stimulated BV2 microglial cells.
Conclusion: These results suggest that MEHC suppresses the induction of TNF-α, as well as iNOS and COX-2 expression, by blocking LPS-induced NF-κB activation.
Keywords: Hydroclathrus clathratus, Nitric oxide, Prostaglandin E2, Tumor necrosis factor-α, Nuclear factor-κB
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.