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Mediators of Inflammation
Volume 2013 (2013), Article ID 787042, 8 pages
Research Article

Radical Scavenging Activity-Based and AP-1-Targeted Anti-Inflammatory Effects of Lutein in Macrophage-Like and Skin Keratinocytic Cells

1Department of Genetic Engineering, Sungkyunkwan University, Suwon 440-746, Republic of Korea
2Department of Food Science and Biotechnology, Sungkyunkwan University, Suwon 440-746, Republic of Korea
3Medical Beauty Research Institute, AmorePacific R&D Center, Yongin 446-729, Republic of Korea
4Sulloccha Research Center, Jangwon. Co., Ltd., Jeju 699-924, Republic of Korea
5Cosmetics & Personal Care Research Division, Amorepacific R&D Center, Yongin 446-729, Republic of Korea

Received 11 December 2012; Accepted 10 January 2013

Academic Editor: Giamila Fantuzzi

Copyright © 2013 Jueun Oh 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.


Lutein is a naturally occurring carotenoid with antioxidative, antitumorigenic, antiangiogenic, photoprotective, hepatoprotective, and neuroprotective properties. Although the anti-inflammatory effects of lutein have previously been described, the mechanism of its anti-inflammatory action has not been fully elucidated. Therefore, in the present study, we aimed to investigate the regulatory activity of lutein in the inflammatory responses of skin-derived keratinocytes or macrophages and to elucidate the mechanism of its inhibitory action. Lutein significantly reduced several skin inflammatory responses, including increased expression of interleukin-(IL-) 6 from LPS-treated macrophages, upregulation of cyclooxygenase-(COX-) 2 from interferon-γ/tumor necrosis-factor-(TNF-) α-treated HaCaT cells, and the enhancement of matrix-metallopeptidase-(MMP-) 9 level in UV-irradiated keratinocytes. By evaluating the intracellular signaling pathway and the nuclear transcription factor levels, we determined that lutein inhibited the activation of redox-sensitive AP-1 pathway by suppressing the activation of p38 and c-Jun-N-terminal kinase (JNK). Evaluation of the radical and ROS scavenging activities further revealed that lutein was able to act as a strong anti-oxidant. Taken together, our findings strongly suggest that lutein-mediated AP-1 suppression and anti-inflammatory activity are the result of its strong antioxidative and p38/JNK inhibitory activities. These findings can be applied for the preparation of anti-inflammatory and cosmetic remedies for inflammatory diseases of the skin.