To fine out the anti-inflammatory activities of the C. fragile. and its mechanism were investigated in macrophages induced by Peptidoglycan (PGN). Treatments of macrophages with 100 ug/ml of ethanol extract of Codium fragile (EECF) inhibited PGN-induced IL-6, NO and PGE2 production in a dose-depende...
To fine out the anti-inflammatory activities of the C. fragile. and its mechanism were investigated in macrophages induced by Peptidoglycan (PGN). Treatments of macrophages with 100 ug/ml of ethanol extract of Codium fragile (EECF) inhibited PGN-induced IL-6, NO and PGE2 production in a dose-dependent manner as well as expression of iNOS and COX-2. EECF inhibited PGN-induced extracellular signal-regulated kinase (ERK) 1/2, JNK 1/2 and p38 MAPK phosphorylation, which suggests that EECF inhibits IL-6 and NO secretion by blocking MAPKs phosphorylation. These findings may help elucidate the mechanism by which EECF modulates RAW 264.7 cell activation under inflammatory conditions.
To fine out the anti-inflammatory activities of the C. fragile. and its mechanism were investigated in macrophages induced by Peptidoglycan (PGN). Treatments of macrophages with 100 ug/ml of ethanol extract of Codium fragile (EECF) inhibited PGN-induced IL-6, NO and PGE2 production in a dose-dependent manner as well as expression of iNOS and COX-2. EECF inhibited PGN-induced extracellular signal-regulated kinase (ERK) 1/2, JNK 1/2 and p38 MAPK phosphorylation, which suggests that EECF inhibits IL-6 and NO secretion by blocking MAPKs phosphorylation. These findings may help elucidate the mechanism by which EECF modulates RAW 264.7 cell activation under inflammatory conditions.
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제안 방법
, 2002). Therefore, the effects of EECF on the PGN-induced phosphorylation of ERK 1/2, JNK 1/2 and p38 MAPK were evaluated in this study. Interestingly, EECF inhibited PGN-induced phosphorylation of ERK 1/2 and p38 MAPK, but phosphorylation of JNK 1/2 was only inhibited at high concentration of EECF (Fig.
To assess the effects of EECF on the PGN-induced PGE2 production in RAW 264.7 cells, cell culture media were harvested and PGE2 levels were measured. To examine whether EECF inhibits PGE2 production, cells were preincubated with EECF for 1 hour and then activated with PGN (30 µg/mL) for 24 hours.
We demonstrated that EECF inhibited PGN-induced proinflammatory mediators, including NO and PGE2. To explore the mechanism of inhibition of NO and PGE2 production in RAW 264.7 cells, the effects of EECF on the iNOS and COX-2 gene were examined. EECF inhibited the expression of COX-2 protein, COX-2 mRNA and iNOS mRNA in a dose-dependent manner, as assessed by Western blot analysis and RT-PCR, respectively.
데이터처리
Statistical significance was compared between each treated group and the control and was determined by Student’s t-tests.
성능/효과
, 2001). The results of this study showed that EECF inhibited PGN-induced NO production in RAW 264.7 macrophages. Taken together, these results indicate that EECF has a potent anti-inflammatory effect that occurs through inhibition of the expression of iNOS and NO production.
후속연구
The fact that EECF has the effect on PGN, its anti-inflammatory activity will be greater against pathogens like MRSA. Therefore, it is possible after further research that EECF could be use against septicemia. Taken together, these findings indicate that EECF may represent a potential new source of drugs for the treatment of inflammatory disease.
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