title: Anti-inflammatory effects of methanol extract of Codium fragile in lipopolysaccharide-stimulated RAW 264.7 cells.
abstract: The methanol extract of Codium fragile (MECF) has been reported to possess bioactive properties such as antidegranulation in eosinophils, as well as anti-edema, antibacterial, and antiviral activities. However, little is known about the molecular effects of MECF on lipopolysaccharide (LPS)-induced inflammation. Therefore, we investigated whether MECF affects the expression of inflammatory mediators in LPS-stimulated RAW 264.7 cells. To evaluate the anti-inflammatory effects of MECF, the cells were pretreated with MECF for 1 hour and then cultured with LPS for 24 hours. Our results indicate that MECF significantly attenuated secretion of LPS-induced inflammatory mediators nitric oxide (NO), prostaglandin E(2) (PGE(2)), and tumor necrosis factor (TNF)-α in RAW 264.7 cells. Additionally, LPS-induced mRNA and protein expression of inducible NO synthase (iNOS), cyclooxygenase (COX)-2, and TNF-α was decreased by pretreatment with MECF. These data indicate that MECF attenuates the expression of these inflammatory mediators at the transcriptional level. Therefore, we also investigated the effects of MECF on nuclear factor-κB (NF-κB) activity, which may be an important transcriptional factor for regulating the expression of iNOS, COX-2, and TNF-α mRNA. Our results showed that MECF reduced LPS-induced NF-κB activity via the suppression of nuclear translocation of the p50 and p65 NF-κB subunits and degradation of inhibitor of κB. In conclusion, we propose that MECF treatment down-regulates the expression and secretion of LPS-induced inflammatory mediators by inhibiting NF-κB activity.
authors.affiliation: Laboratory of Immunobiology, Department of Marine Life Sciences, Jeju National University, Jeju, Korea.
authors.forename: Chang-Hee
authors.initials: CH
authors.lastname: Kang
authors.forename: Yung Hyun
authors.initials: YH
authors.lastname: Choi
authors.forename: Sung-Yong
authors.initials: SY
authors.lastname: Park
authors.forename: Gi-Young
authors.initials: GY
authors.lastname: Kim
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology / Q000627:therapeutic use*; D001692:Biological Transport / Q000187:drug effects; D002460:Cell Line; D002467:Cell Nucleus; D000460:Chlorophyta; D051546:Cyclooxygenase 2 / Q000235:genetics / Q000378:metabolism; D015536:Down-Regulation; D015870:Gene Expression / Q000187:drug effects*; D007249:Inflammation / Q000188:drug therapy* / Q000378:metabolism; D018836:Inflammation Mediators / Q000378:metabolism*; D008070:Lipopolysaccharides; D051379:Mice; D016328:NF-kappa B / Q000378:metabolism*; D052247:Nitric Oxide Synthase Type II / Q000235:genetics / Q000378:metabolism; D010936:Plant Extracts / Q000494:pharmacology / Q000627:therapeutic use*; D012333:RNA, Messenger / Q000378:metabolism; D014157:Transcription Factors / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000378:metabolism
chemical_list: D000893:Anti-Inflammatory Agents; D018836:Inflammation Mediators; D008070:Lipopolysaccharides; D016328:NF-kappa B; D010936:Plant Extracts; D012333:RNA, Messenger; D014157:Transcription Factors; D014409:Tumor Necrosis Factor-alpha; D052247:Nitric Oxide Synthase Type II; D051546:Cyclooxygenase 2