Abstract
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 accelerates cutaneous 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 rate was 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.
Highlights
Wound healing is an essential procedure that helps maintain homeostasis and integrate tissue injured by physical, chemical, bacterial, or viral insults [1,2,3]
Dietary Conjugated linoleic acid (CLA) supplementation significantly reduced the body weights gain in mice throughout the experimental periods compared to a control diet (Figure 1)
Body weight gain was lower in the 1% CLAsupplemented group than the control and 0.5% CLAsupplemented groups (P < .05)
Summary
Wound healing is an essential procedure that helps maintain homeostasis and integrate tissue injured by physical, chemical, bacterial, or viral insults [1,2,3]. 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 period that regulates the entire healing process [5,6,7]. IL-1β and TNF-α, primary proinflammatory cytokines, promote nuclear factor κB (NFκB) activation and ROS production in inflammatory cells [8,9,10]. 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
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