Abstract
BackgroundDiabetic foot ulcers are serious complications for diabetic patients, yet the precise mechanism that underlines the treatment of these diabetic complications remains unclear. We hypothesized that dietary antioxidant supplementation with vitamin C, combined either with vitamin E or with vitamin E and NAC, improves delayed wound healing through modulation of blood glucose levels, oxidative stress, and inflammatory response.MethodsDiabetes was induced by administration of alloxan monohydrate. Mice were divided into 4 groups; CON (non-diabetic control mice fed AIN 93 G purified rodent diet), DM (diabetic mice fed AIN 93 G purified rodent diet), VCE (diabetic mice fed 0.5% vitamin C and 0.5% vitamin E supplemented diet), and Comb (diabetic mice fed 0.5% vitamin C, 0.5% vitamin E, and 2.5% NAC supplemented diet). After 10 days of dietary antioxidant supplementation, cutaneous full-thickness excisional wounds were performed, and the rate of wound closure was examined. TBARS as lipid peroxidation products and vitamin E levels were measured in the liver. Expression levels of oxidative stress and inflammatory response related proteins were measured in the cutaneous wound site.ResultsDietary antioxidant supplementation improved blood glucose levels and wound closure rate and increased liver vitamin E, but not liver TBARS levels in the diabetic mice as compared to those of the CON. In addition, dietary antioxidant supplementation modulated the expression levels of pIκBα, HO-1, CuZnSOD, iNOS and COX-2 proteins in the diabetic mice.ConclusionsThese findings demonstrated that delayed wound healing is associated with an inflammatory response induced by hyperglycaemia, and suggests that dietary antioxidant supplementation may have beneficial effects on wound healing through selective modulation of blood glucose levels, oxidative stress, and inflammatory response.
Highlights
Diabetes mellitus (DM) is a disease in which injury of peripheral tissue is induced by oxidative stress caused by chronic hyperglycaemia
To examine the change of the inflammatory response by dietary antioxidant supplementation at molecular levels that modify the rate of the wound closure, we investigated the expressions of oxidative stress and inflammatory response related proteins
The results in this study suggest that dietary antioxidant supplementation creates synergetic effects that improve the condition of diabetes through the regulation of blood glucose levels and effects that accelerate the early inflammatory responses during cutaneous wound healing
Summary
Diabetes mellitus (DM) is a disease in which injury of peripheral tissue is induced by oxidative stress caused by chronic hyperglycaemia. The first stage in the wound healing process, neutrophils and macrophages infiltrate the wound site and phagocytose infectious agents and fragments of tissue degradation release proteases and various reactive oxygen species (ROS) into the wound environment [2]. They are both major sources and targets of pro-inflammatory cytokines such as IL-1b and TNF-a, which have been shown to be key mediators by promoting NFB activation and ROS production during cutaneous inflammatory processes [3]. We hypothesized that dietary antioxidant supplementation with vitamin C, combined either with vitamin E or with vitamin E and NAC, improves delayed wound healing through modulation of blood glucose levels, oxidative stress, and inflammatory response
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
