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Tropical Journal of Pharmaceutical Research
Pharmacotherapy Group, Faculty of Pharmacy, University of Benin, Benin City, Nigeria
ISSN: 1596-5996
EISSN: 1596-5996
Vol. 10, No. 6, 2011, pp. 723-730
Bioline Code: pr11086
Full paper language: English
Document type: Research Article
Document available free of charge

Tropical Journal of Pharmaceutical Research, Vol. 10, No. 6, 2011, pp. 723-730

 en Methanol Extract of Hydroclathrus clathratus check for this species in other resources Inhibits Production of Nitric Oxide, Prostaglandin E2 and Tumor Necrosis Factor-α in Lipopolysaccharidestimulated BV2 Microglial Cells via Inhibition of NF-κB Activity
Jayasooriya, RGPT; Moon, Dong-Oh; Choi, Yung Hyun; Yoon, Chang-Hoon & Kim, Gi-Young


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.

Hydroclathrus clathratus, Nitric oxide, Prostaglandin E2, Tumor necrosis factor-α, Nuclear factor-κB

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