Bioelectromagnetics Pulsed Electromagnetic Fields Accelerate Wound Healing in the Skin of Diabetic Rats Iran Goudarzi, 1,2 * Sohrab Hajizadeh, 1 Mahmoud E. Salmani, 2 and Kataneh Abrari 2 1 FacultyofMedicalSciences,DepartmentofPhysiology,TarbiatModaresUniversity, Tehran,Iran 2 DepartmentofBiology,DamghanUniversityofBasicSciences,Damghan,Iran Delayed wound healing is a common complication in diabetes mellitus. From this point of view, the main purpose of the present study is to investigate the effect of extremely low frequency pulsed electromagnetic fields (ELF PEMFs) on skin wound healing in diabetic rats. In this study, diabetes was induced in male Wistar rats via a single subcutaneous injection of 65 mg/kg streptozocin (freshly dissolved in sterile saline, 0.9%). One month after the induction of diabetes, a full-thickness dermal incision (35 mm length) was made on the right side of the paravertebral region. The wound was exposed to ELF PEMF (20 Hz, 4 ms, 8 mT) for 1 h per day. Wound healing was evaluated by measuring surface area, percentage of healing, duration of healing, and wound tensile strength. Obtained results showed that the duration of wound healing in diabetic rats in comparison with the control group was significantly increased. In contrast, the rate of healing in diabetic rats receiving PEMF was significantly greater than in the diabetic control group. The wound tensile strength also was significantly greater than the control animals. In addition, the duration of wound healing in the control group receiving PEMF was less than the sham group. Based on the above-mentioned results we concluded that this study provides some evidence to support the use of ELF PEMFs to accelerate diabetic wound healing. Further research is needed to determine the PEMF mechanisms in acceleration of wound healing in diabetic rats. Bioelectromagnetics. ß 2010 Wiley-Liss, Inc. Key words: wound healing; pulsed electromagnetic field; streptozocin; diabetes; rat INTRODUCTION Chronic wounds affect a large proportion of the population and result in tremendous costs, both in human suffering and in actual health care dollars expended to treat the problem [Leigh and Bennett, 1994; Phillips et al., 1994]. Diabetes Mellitus (DM) markedly increases the risk of lower extremity ulcer- ation, and chronic hyperglycemia is responsible for the development of many of the complications in DM [Brownlee, 1992]. However, the exact nature of the pathogenesis of poor wound healing in diabetes is not completely understood. Evidence from studies involving both human and animal models of diabetes reveal several abnormalities in various phases of the wound-healing process. Diabetes-induced impairment of wound healing is characterized by inhibition of inflammatory response, angiogenesis, fibroplasias, defects in collagen deposition and differentiation of extracellular matrix [Prakash et al., 1974; Goodson and Hunt, 1977, 1979; Fahey et al., 1991]. Previous studies showed that electrical stimulation applied to full- thickness excisional wounds in mice with alloxan monohydrate-induced DM produced a reduction in wound size [Thawer and Houghton, 1999; Thawer et al., 2000]. Human clinical trials and animal experiments have shown that electrical stimulation of skin accel- erates wound healing, presumably by augmenting the endogenous current induced by injury [Reich and Tarjan, 1990; Weiss et al., 1990; Mulder, 1991]. However, direct current (DC) stimulation used in these studies has the disadvantage of requiring electrode placement directly on or near the wound. Pulsed electromagnetic fields (PEMFs) have an inherent advantage over DC systems in that the electromagnetic signal penetrates the dressing and tissue involved. In short, pulsed magnetic fields interact ß 2010 Wiley-Liss, Inc. —————— *Correspondence to: I. Goudarzi, Department of Biology, Damghan University of Basic Sciences, 3671641167, Damghan, Iran. E-mail: irangoudarzi@yahoo.com Received for review 10 January 2009; Accepted: 17 November 2009 DOI 10.1002/bem.20567 Published online in Wiley InterScience (www.interscience.wiley.com).