Please use this identifier to cite or link to this item: http://hdl.handle.net/10397/28156
Title: Pulsed electromagnetic fields (PEMF) promote early wound healing and myofibroblast proliferation in diabetic rats
Authors: Cheing, GLY 
Li, X
Huang, L
Kwan, RLC
Cheung, KK
Keywords: Collagen
Diabetes
Epithelialization
PEMF
Pulsed electromagnetic fields
Tensile strength
Wound closure
Issue Date: 2014
Publisher: John Wiley & Sons
Source: Bioelectromagnetics, 2014, v. 35, no. 3, p. 161-169 How to cite?
Journal: Bioelectromagnetics 
Abstract: Reduced collagen deposition possibly leads to slow recovery of tensile strength in the healing process of diabetic cutaneous wounds. Myofibroblasts are transiently present during wound healing and play a key role in wound closure and collagen synthesis. Pulsed electromagnetic fields (PEMF) have been shown to enhance the tensile strength of diabetic wounds. In this study, we examined the effect of PEMF on wound closure and the presence of myofibroblasts in Sprague-Dawley rats after diabetic induction using streptozotocin. A full-thickness square-shaped dermal wound (2cm×2cm) was excised aseptically on the shaved dorsum. The rats were randomly divided into PEMF-treated (5mT, 25Hz, 1h daily) and control groups. The results indicated that there were no significant differences between the groups in blood glucose level and body weight. However, PEMF treatment significantly enhanced wound closure (days 10 and 14 post-wounding) and re-epithelialization (day 10 post-wounding), although these improvements were no longer observed at later stages of the wound healing process. Using immunohistochemistry against α-smooth muscle actin (α-SMA), we demonstrated that significantly more myofibroblasts were detected on days 7 and 10 post-wounding in the PEMF group when compared to the control group. We hypothesized that PEMF would increase the myofibroblast population, contributing to wound closure during diabetic wound healing.
URI: http://hdl.handle.net/10397/28156
ISSN: 0197-8462
EISSN: 1521-186X
DOI: 10.1002/bem.21832
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