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Toxicol Res
2010 Mar 01;261:37-46. doi: 10.5487/tr.2010.26.1.037.
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Methanolic Extract of Asterina pectinifera inhibits LPS-Induced Inflammatory Mediators in Murine Macrophage.
Jo WS
,
Choi YJ
,
Kim HJ
,
Nam BH
,
Lee GA
,
Seo SY
,
Lee SW
,
Jeong MH
.
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This study aimed to elucidate anti-inflammatory activities from extracts of Asterina pectinifera on nitric oxide (NO) production, TNF-α and IL-6 release in lipopolysaccharide (LPS) -stimulated murine macrophage cell, RAW264.7. We prepared the methanolic extracts (60-MAP, 70-MAP, 80-MAP and 90-MAP) , aqueous extract (W-AP) and functional bioactive compound fraction (He-AP and EA-AP) from Asterina pectinifera according to extract method. The 60-MAP, 70-MAP, 80-MAP, 90-MAP and W-AP were significantly suppressed LPS-induced production NO, TNF-α and IL-6 secretion in a concentration-dependent manner (P < 0.05) . Especially, 80-MAP by extracted 80% methanol had the strongest activity in reduction of inflammatory mediators among these extracts. Indeed, to identify active fraction, which contained potential bioactive compounds, from 80-MAP of Asterina pectinifera, we tested anti-inflammatory activity of the He-AP or the EA-AP. The He-AP was next extracted from 80-MAP and the EA-AP were extracted from the other methanol layer except the He-AP. The EA-AP demonstrated a strong anti-inflammatory effect through its ability to reduce NO production and it also inhibited the production of proinflammatory cytokines such as IL-6 and TNF-α at low concentration. These results suggested that the methanolic extract from Asterina pectinifera had the potential inhibitory effects on the production of these inflammatory mediators.
Fig. 1. Procedure for extraction or fraction of bioactive compounds from Asterina pectinifera. The extractive procedures were described in (A) the methnolic extraction, (B) the aqueous extraction and (C) the hexane fraction or ethyl acetate fraction according to extract method from Asterina pectinifera.
Fig. 2. Cytotoxicity of extracts from Asterina pectinifera in RAW 264.7 cell. RAW 264.7 cells were treated with each concentration of the methnolic extracts (60-MAP 70-MAP 80-MAP and 90-MAP) and aqueous extract (W-AP) from Asterina pectinifera (A) , hexane fraction (He-AP) and ethyl acetate fraction (EA-AP) (B) for 24 h. Cell viability was determined by MTT assay. Three independent assays were performed in triplicate and the data shown are the mean ± SD.
Fig. 3. Effects of the methanolic and aqueous extract from Asterina pectinifera on LPS-induced nitirc oxide (NO) in murine macrophages. RAW 264.7 cells were treated with concentrations of methanolic and aqueous extract from Asterina pectinifera (60-MAP 70-MAP 80-MAP 90-MAP and W-AP) in the presence of 500 ng/ml of LPS or LPS alone for 24 h. L-NMMA was used as a positive control. Three independent assays were performed in triplicate and the data shown are the mean ± S.D. *P < 0.05 vs. media alone and #P < 0.05 vs. LPS-treated group (control) ; significance of difference between treated groups by Students-t tests (*) and ANOVA followed by Dunnett’s test (#) .
Fig. 6. Effects by active compound fraction from 80-MAP of Asterina pectinifera on LPS-induced nitirc oxide (NO) IL-6 production and TNF-α production in murine macrophages. RAW 264.7 cells were treated with concentrations of hexane fraction (He-AP) and ethyl acetate fraction (EA-AP) in the presence of 500 ng/ml of LPS or LPS alone for 24 h. The production of NO was evaluated by Griess reaction (A) . The concentration of IL-6 (B) and TNF-α (C) in condition medium was analyzed by ELISA. Three independent assays were performed in triplicate and the data shown are the mean ± S.D. *P< 0.05 vs. media alone and #P < 0.05 vs. LPS-treated group (control) ; significance of difference between treated groups by Students-t tests (*) and ANOVA followed by Dunnett’s test (#) .
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