Methanol Extract of
Hydroclathrus clathratus Inhibits Production of
Nitric Oxide, Prostaglandin E2 and Tumor
Necrosis Factor-α in Lipopolysaccharide-stimulated BV2
Microglial Cells via Inhibition of NF-κB Activity
RGPT Jayasooriya1,
Dong-Oh Moon2, Yung Hyun Choi3,
Chang-Hoon Yoon4, and Gi-Young Kim1*
1
Laboratory of
Immunobiology, Department of Marine Life Sciences, Jeju
National University, Jeju 690-756, 2
Department of Biology Education, College of Education,
Gyeongsan, Gyeongbuk 712-714, 3 Department of
Biochemistry, College of Oriental Medicine, Dongeui
University, Busan 614-054, 4 Department of
Food and Nutrition, College of Natural Science, Jeju
National University, 690-756, Republic of Korea.
For correspondence:
E-mail:
immunkim@jejunu.ac.kr Tel: +82 64 754
3427; Fax: +82 64 756 3493
Received: 4 March
2011
Revised accepted: 16 September, 2011
Tropical
Journal of Pharmaceutical Research, December 2011;
10(6): 723-730
http://dx.doi.org/10.4314/tjpr.v10i6.4
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.
