Article Sidebar
Published:
Mar 7, 2013Keywords:
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
Inhibition of Nitric Oxide and Prostaglandin E2 Expression by Methanol Extract of Polyopes affinis in Lipopolysaccharide-stimulated BV2 Microglial Cells through Suppression of Akt-dependent NF-kB Activity and MAPK Pathway
Abstract
Purpose: To determine whether the methanol extract of Polyopes affinis (MEPA) down-regulates the expression of pro-inflammatory mediators in lipopolysaccharide (LPS)-stimulated BV2 microglial cells.
Methods: The production of nitric oxide (NO) and prostaglandin E2 (PGE2) was measured by the Griess reagents and enzyme-linked immunosorbent assay (ELISA), respectively. Expression levels of mRNA and protein in LPS-stimulated BV2 microglial cells were assessed by reverse transcription-polymerase (RT-PCR) and Western blot analysis. Activation of nuclear factor-êB (NF-êB) was detected by electrophoretic mobility shift assay (EMSA).
Results: MEPA inhibited the expression of LPS-induced pro-inflammatory mediators, NO and PGE2, as well as their respective genes, iNOS and COX-2, at both protein and mRNA levels, without any accompanying cytotoxicity. Moreover, treatment with MEPA significantly suppressed the LPS-induced DNA-binding activity of NF-êB, which is known as a main transcription factor for the regulation of proinflammatory genes, as well as the nuclear translocation of its subunit p65 and p50, by degrading IêBá.
MEPA increased Akt dephosphorylation which leads to suppression of the DNA-binding activity of NF-kB in LPS-stimulated BV2 microglial cells and suppressed phosphorylation of ERK and JNK, which are involved in the mitogen-activated protein kinase (MAPK) signaling pathway for regulating proinflammatory genes.
Conclusion: Our results indicate that MEPA down-regulates pro-inflammatory mediators such as NO and PGE2 by suppressing Akt-dependent NF-êB activity as well as phosphorylation of ERK and JNK in
LPS-stimulated BV2 microglial cells.
Keywords: Polyopes affinis, Nitric oxide, Prostaglandin E2, Nuclear factor-kB
