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Tropical Journal of Pharmaceutical Research
Pharmacotherapy Group, Faculty of Pharmacy, University of Benin, Benin City, Nigeria
ISSN: 1596-5996
EISSN: 1596-9827
Vol. 11, No. 6, 2012, pp. 917-924
Bioline Code: pr12108
Full paper language: English
Document type: Research Article
Document available free of charge

Tropical Journal of Pharmaceutical Research, Vol. 11, No. 6, 2012, pp. 917-924

 en Methanol Extract of Myelophycus caespitosus check for this species in other resources Inhibits the Inflammatory Response in Lipopolysaccharidestimulated BV2 Microglial Cells by Downregulating NF-κB via Inhibition of the Akt Signaling Pathway
Jayasooriya, Rajapaksha Gendara Prasad Tharanga; Kang, Chang-Hee; Jang, Yeon-Jeong; Kang, Sang-Hyuck; Dilshara, Matharage Gayani; Choi, Yung Hyun; Moon, Dong-Oh & Kim, Gi-Young

Abstract

Purpose: To determine whether the methanol extract of Myelophycus caespitosus check for this species in other resources (MEMC) downregulates the expression of pro-inflammatory mediators in lipopolysaccharide (LPS)-stimulated BV2 microglial cells.
Methods: Reverse transcription-polymerase chain reaction (RT-PCR) together with Western blot analysis was used to evaluate the expression of pro-inflammatory mediators such as nitric oxide (NO) and prostaglandin E2 (PGE2) as well as their regulatory genes such as inducible NO synthase (iNOS) and cyclooxygenase-2 (COX- 2), in LPS-stimulated BV2 microglial cells. The level of NO production was analyzed using Griess reaction. The release of PGE2 was determined using sandwich enzyme-linked immunosorbent assay. The DNA-binding activity of nuclear factor-κB (NF-κB) was measured by electrophoretic mobility shift assay.
Results:MEMC inhibited 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 significant cytotoxicity. Treatment with MEMC also substantially reduced the LPS-induced DNA-binding activity of NF-κB and nuclear translocation of NF-κB subunits p65 and p50 via the inhibition of IκBa phosphorylation and degradation. MEMC promoted dephosphorylation of Akt that subsequently suppressed the DNA-binding activity of NF-κB in LPS-stimulated BV2 microglial cells.
Conclusion: Collectively, these data suggest that MEMC attenuates expression of pro-inflammatory mediators such as NO and PGE2 by suppression of their regulatory genes through the inhibition of Aktmediated NF-κB activity.

Keywords
Myelophycus caespitosus, Nitric oxide, Prostaglandin E2, Nuclear factor-κB

 
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