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Evidence-Based Complementary and Alternative Medicine
Volume 2013 (2013), Article ID 747846, 10 pages
http://dx.doi.org/10.1155/2013/747846
Research Article

Sargassum fulvellum Protects HaCaT Cells and BALB/c Mice from UVB-Induced Proinflammatory Responses

1Department of Pharmacology, School of Medicine, Keimyung University, 2800 Dalgubeoldaero, Dalseo-gu, Daegu 704-701, Republic of Korea
2Research Institute of Pharmaceutical Sciences, College of Pharmacy, Kyungpook National University, Daegu 702-701, Republic of Korea
3Department of Herbal Foodceutical Science, Daegu Haany University, Gyeongsangbuk-do 712-230, Republic of Korea
4Department of Cosmeceutical Science, Daegu Haany University, 290 Yugok-dong, Gyeongsan-si, Gyeongsangbuk-do 712-230, Republic of Korea

Received 29 November 2012; Accepted 10 June 2013

Academic Editor: Vernon A. Barnes

Copyright © 2013 Chan Lee et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Ultraviolet (UV) radiation has been reported to induce cutaneous inflammation such as erythema and edema via induction of proinflammatory enzymes and mediators. Sargassum fulvellum is a brown alga of Sargassaceae family which has been demonstrated to exhibit antipyretic, analgesic, antiedema, antioxidant, antitumor, fibrinolytic, and hepatoprotective activities. The purpose of this study is to investigate anti-inflammatory effects of ethylacetate fraction of ethanol extract of Sargassum fulvellum (SFE-EtOAc) in HaCaT keratinocytes and BALB/c mice. In HaCaT cells, SFE-EtOAc effectively inhibited UVB-induced cytotoxicity (60 mJ/cm2) and the expression of proinflammatory proteins such as cyclooxygenase-2 (COX-2), tumor necrosis factor- (TNF- ), and inducible nitric oxide synthase (iNOS). Furthermore, SFE-EtOAc significantly reduced UVB-induced production of proinflammatory mediators including prostaglandin E2 (PGE2) and nitric oxide (NO). In BALB/c mice, topical application of SFE-EtOAc prior to UVB irradiation (200 mJ/cm2) effectively suppressed the UVB-induced protein expression of COX-2, iNOS, and TNF- and subsequently attenuated generation of PGE2 and NO as well. In another experiment, SFE-EtOAc pretreatment suppressed UVB-induced reactive oxygen species production and exhibited an antioxidant potential by upregulation of antioxidant enzymes such as catalase and Cu/Zn-superoxide dismutase in HaCaT cells. These results suggest that SFE-EtOAc could be an effective anti-inflammatory agent protecting against UVB irradiation-induced skin damages.