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Pages: 25 (6177 mots) Publié le: 31 janvier 2011
Hindawi Publishing Corporation Mediators of Inflammation Volume 2010, Article ID 342328, 8 pages doi:10.1155/2010/342328

Research Article Effect of Dietary Conjugated Linoleic Acid Supplementation on Early Inflammatory Responses during Cutaneous Wound Healing
Na-Young Park, Giuseppe Valacchi, and Yunsook Lim
Department of Food and Nutrition, Research Institute of Science for Human Life, KyungHee University, 1 Hoegi-dong, Dongdaemun-gu, Seoul 130-761, Republic of Korea Correspondence should be addressed to Yunsook Lim, ylim@khu.ac.kr Received 22 January 2010; Accepted 6 July 2010 Academic Editor: Chiara De Luca Copyright © 2010 Na-Young Park 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. Inflammatory response is considered the most important period that regulates the entire healing process. Conjugated linoleic acid (CLA), a class of linoleic acid positional and geometric isomers, is well known for its antioxidant and anti-inflammatory properties. We hypothesized that dietary CLA supplementation acceleratescutaneous wound healing by regulating antioxidant and anti-inflammatory functions. To investigate wound closure rates and inflammatory responses, we used a full-thickness excisional wound model after 2-week treatments with control, 0.5%, or 1% CLA-supplemented diet. Mice fed dietary CLA supplementation had reduced levels of oxidative stress and inflammatory markers. Moreover, the wound closure ratewas improved significantly in mice fed a 1% CLA-supplemented diet during early stage of wound healing (inflammatory stage). We conclude that dietary CLA supplementation enhances the early stage of cutaneous wound healing as a result of modulating oxidative stress and inflammatory responses.

1. Introduction
Wound healing is an essential procedure that helps maintain homeostasis and integrate tissueinjured by physical, chemical, bacterial, or viral insults [1–3]. Generally, there are three major stages of wound healing that overlap in time and space: inflammation, proliferation, and remodeling [4]. Because it is involved in producing growth factors and cytokines that coordinate the cell and tissue movements necessary for repair, the inflammatory response is considered the most important periodthat regulates the entire healing process [5– 7]. The initial event of the inflammatory stage during wound healing is the infiltration of neutrophils and macrophages into the wound site to attack contaminating bacteria and to phagocytose cellular debris resulting in the production of reactive oxygen species (ROS). Furthermore, neutrophils and macrophages are both major sources and targets ofproinflammatory cytokines such as IL-1α, IL-1β, IL-6, and TNF-α that have been shown to be crucial mediators during cutaneous inflammatory processes [4, 5]. For example, IL-1β and TNF-α, primary proinflammatory cytokines, promote nuclear factor κB (NFκB) activation and ROS production in inflammatory cells [8–10]. NFκB is a redox-sensitive

transcription factor that acts as a central protein regulating thetranscription of many inflammatory mediators including cyclooxygenase (COX)-2, a rate-limiting enzyme in the biosynthesis of prostaglandins during inflammation and immune response. Because of its essential role in controlling inflammatory responses, regulation of NFκB activation by the oxidative stress present during the early inflammatory cascade may be advantageous in the treatment of wounds. Cellsin injured and inflamed tissues are able to protect themselves with a well-equipped array of antioxidant enzymes, such as glutathione peroxidase (GPX), catalase, superoxide dismutases (SODs), and heme oxygenases (HO). SODs dismutate superoxide radical anions to H2 O2 and water. A previous study has shown that mRNA levels of CuZnSOD and MnSOD were upregulated in the early inflammatory stage of...
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