title: Protective effect of Codium fragile against UVB-induced pro-inflammatory and oxidative damages in HaCaT cells and BALB/c mice.
abstract: Acute exposure to ultraviolet (UV) radiation causes pro-inflammatory responses via diverse mechanisms including oxidative stress. Codium fragile is a green alga of Codiales family and has been reported to exhibit anti-edema, anti-allergic, anti-protozoal and anti-mycobacterial activities. In this study, we have investigated a novel anti-inflammatory potential of C. fragile using in vitro cell culture as well as in vivo animal models. In HaCaT cells, buthanol and ethylacetate fractions of 80% methanol C. fragile extract (CFB or CFE) and a single compound, clerosterol (CLS) isolated from CFE attenuated UVB (60 mJ/cm(2))-induced cytotoxicity and reduced expression of pro-inflammatory proteins including cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), and tumor necrosis factor-α (TNF- α). Moreover, CFB, CFE and CLS effectively suppressed UVB-induced production of pro-inflammatory mediators such as prostaglandin E2 (PGE2) and nitric oxide (NO). In another experiment, topical application of CFB, CFE or CLS prior to UVB irradiation (200 mJ/cm(2)) on BALB/c mice, inhibited the UVB-elevated protein levels of COX-2, iNOS, and TNF-α. Furthermore, CFB, CFE and CLS suppressed oxidative damages caused by UVB irradiation for example lipid peroxidation and/or protein carbonylation, which seemed to be mediated by up-regulation of antioxidant defense enzymes. These results suggest that C. fragile could be an effective therapeutic agent providing protection against UVB-induced inflammatory and oxidative skin damages.
authors: Department of Pharmacology, School of Medicine, Keimyung University, Daegu 704-701, South Korea.
authors: Chan
authors: C
authors: Lee
authors: Gyu Hwan
authors: GH
authors: Park
authors: Eun Mi
authors: EM
authors: Ahn
authors: Bo-Ae
authors: BA
authors: Kim
authors: Chan-Ik
authors: CI
authors: Park
authors: Jung-Hee
authors: JH
authors: Jang
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology / Q000627:therapeutic use; D000975:Antioxidants / Q000494:pharmacology / Q000627:therapeutic use; D002460:Cell Line; D000460:Chlorophyta / Q000737:chemistry*; D051546:Cyclooxygenase 2 / Q000378:metabolism; D052246:Cyclooxygenase 2 Inhibitors / Q000494:pharmacology / Q000627:therapeutic use; D006801:Humans; D007249:Inflammation / Q000188:drug therapy* / Q000209:etiology / Q000378:metabolism; D018836:Inflammation Mediators / Q000378:metabolism; D015603:Keratinocytes / Q000187:drug effects / Q000378:metabolism / Q000528:radiation effects; D015227:Lipid Peroxidation / Q000187:drug effects; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D052247:Nitric Oxide Synthase Type II / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects*; D008517:Phytotherapy; D010936:Plant Extracts / Q000494:pharmacology / Q000627:therapeutic use*; D050050:Protein Carbonylation / Q000187:drug effects; D011832:Radiation Injuries / Q000188:drug therapy* / Q000378:metabolism; D012867:Skin / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism / Q000528:radiation effects; D012871:Skin Diseases / Q000188:drug therapy* / Q000209:etiology / Q000378:metabolism; D013256:Steroids / Q000302:isolation & purification / Q000494:pharmacology / Q000627:therapeutic use; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D014466:Ultraviolet Rays / Q000009:adverse effects
chemical_list: D000893:Anti-Inflammatory Agents; D000975:Antioxidants; D052246:Cyclooxygenase 2 Inhibitors; D018836:Inflammation Mediators; D010936:Plant Extracts; D013256:Steroids; D014409:Tumor Necrosis Factor-alpha; C583592:clerosterol; D052247:Nitric Oxide Synthase Type II; D051546:Cyclooxygenase 2