Methanol Extract of
Polyopes lancifolius
Inhibits the Expression of Pro-inflammatory Mediators in
LPS-stimulated BV2 Microglia Cells via Downregulation of
the
NF-κB Pathway
RGPT Jayasooriya1, Chang-Hee Kang1,
Sung-Yong Park2, Yung Hyun Choi3,
Dong-Oh Moon4 and Gi-Young Kim1*
1Laboratory
of Immunobiology, Department of Marine Life Sciences,
Jeju National University, Jeju 690-756,
2OTTOGI
Research Institute, OTTOGI Ltd., Gyeonggi-do 431-070,
3Department of Biochemistry, College of
Oriental Medicine, Dongeui University, Busan 614-054,
4Department of Biology Education, College of
Education, Gyeongsan, Gyeongbuk 712-714, Republic of
Korea.
*For
correspondence:
Email:
immunkim@jejunu.ac.kr
Tel: +82 64 754 3427; Fax: +82 64 756 3493
Received: 1 April
2011 Revised
accepted: 11 December 2011
Tropical Journal of
Pharmaceutical Research, February 2012; 11(1): 43-50
http://dx.doi.org/10.4314/tjpr.v11i1.6
Abstract
Purpose:
This study is aimed at identifying the anti-inflammatory
mechanisms of a methanol extract of Polyopes lancifolius
(MEPL) in lipopolysaccharide (LPS)-stimulated BV2
microglia cells.
Methods: The
expression of mRNA and protein were investigated RT-PCR
and western blot analyses in 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:
MEPL significantly suppressed NO production in
LPS-stimulated BV2 cells without any cytotoxicity. The
results also indicate that MEPL decreased the production
of PGE2 and TNF-α in LPS-stimulated BV2
cells. Furthermore, pretreatment with MEPL resulted in a
downregulation of LPS-induced mRNA and protein
expression of inducible NO synthase (iNOS),
cyclooxygenase-2 (COX-2) and TNF-α. Investigation of the
effect of MEPL on nuclear factor-κB (NF-κB) activity,
which is a potential transcriptional factor for
regulating inflammatory genes such as iNOS, COX-2 and
TNF-α, showed that MEPL substantially inhibited the
LPS-induced DNA-binding activity of NF-κB. MEPL also
suppressed the LPS-induced degradation and
phosphorylation of IκBα, and it consequently blocked p65
translocation from the cytosol to the nucleus.
Conclusion:
These data show that MEPL may regulate LPS-induced NO,
PGE2, and TNF-α production by
suppressing NF-κB activity.
Keywords:
Polyopes lancifolius,
Nitric oxide, Prostaglandin E2, Tumor
necrosis factor-α,
Nuclear factor-κB
