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, firstname.lastname@example.org 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.
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 . 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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