Anti-inflammatory effect of Papenfussiella kuromo in lipopolysaccharide or peptidoglycan-induced macrophage cells
Author(s) -
OkHwa Kang
Publication year - 2012
Publication title -
african journal of pharmacy and pharmacology
Language(s) - English
Resource type - Journals
ISSN - 1996-0816
DOI - 10.5897/ajpp12.226
Subject(s) - mapk/erk pathway , lipopolysaccharide , nitric oxide , kinase , peptidoglycan , nitric oxide synthase , chemistry , signal transduction , western blot , microbiology and biotechnology , protein kinase a , biochemistry , pharmacology , enzyme , biology , immunology , organic chemistry , gene
Marine bioresources are known to be attractive as they sometimes contain new compounds showing several kinds of different bioactivities which are not possible in land plants. Brown algae, Papenfussiella kuromo is widely distributed in Korea and Japan. However, no studies have been conducted to evaluate the anti-inflammatory activities of the extract of P. kuromo. We studied its anti-inflammatory effect in Peptidoglycan (PGN)- and lipopolysaccharide (LPS)-induced RAW 264.7 macrophage cells activation. In the present study, interleukin (IL)-6 productions was measured using the enzyme-linked immunosorbent assay (ELISA), prostaglandin (PG) E2 production was measured using the enzyme immunosorbent assay(EIA) kit and mitogen-activated protein kinase (MAPK) activation, as determined by western blot analysis and reverse transcription-polymerase chain reaction (RT-PCR). P. kuromoinhibited PGN-induced IL-6 production in a dose-dependent manner and also inhibited LPS-induced IL-6 production. Additionally, P. kuromo caused significant inhibition of both PGN- and LPS-induced PGE2 expression. P. kuromo significantly inhibited PGN-induced extracellular signal-regulated kinase (ERK) 1/2 phosphorylation. Conclusively, P. kuromo inhibited nitrite oxide (NO), PGE2 secretion and inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2) expression by blocking ERK 1/2 phosphorylation in LPS- or PGN-induced RAW 264.7 cells. The results clarify the similarity and difference between PGN- and LPS-mediated signal transduction and induction of inflammatory cytokine in macrophages. Taken together, these findings may help to elucidate the mechanism by which P. kuromo modulates RAW 264.7 cell activation under inflammatory conditions. Key words: Papenfussiella kuromo, peptidoglycan (PGN), lipopolysaccharide (LPS), macrophages.
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