title: High-voltage pulsed current stimulation enhances wound healing in diabetic rats by restoring the expression of collagen, α-smooth muscle actin, and TGF-β1.
abstract: Impaired wound healing is a common complication of diabetes mellitus and a major morbidity that leads to pain and severely diminished quality of life. Diabetic wounds are commonly associated with defective immune cell responses or abnormality of extracellular matrix. Various types of electrical stimulation interventions have been used to promote tissue healing. However, it is unclear whether high-voltage pulsed current stimulation (HVPCS) enhances diabetic wound healing. In this study, the effects of HVPCS on wound healing were investigated in diabetic rats. Three groups of rats (10 per group) were used: non-diabetic control, diabetic control, and diabetic rats that were administered HVPCS for 40 minutes daily for 1 week. Rats from control groups were administered sham interventions. Dorsal incision wounds were generated in all animals, and wound-healing rate was determined during one-week intervention. After interventions, we measured the relative expression levels of collagen type I (collagen-I), α-smooth muscle actin (α-SMA), and transforming growth factor-β1 (TGF-β1) mRNAs in the wounded skin. Wound closure was delayed in diabetic control rats compared to the non-diabetic control rats, and the diabetic control rats showed the reduced expression levels of collagen-I, α-SMA and TGF-β1 mRNAs. Importantly, compared to diabetic control rats, rats with HVPCS showed accelerated wound closure and healing (p < 0.01) and restored expression levels of collagen-I (p = 0.02), α-SMA (p = 0.04), and TGF-β1 (p = 0.01) mRNAs. In conclusion, HVPCS may be beneficial for enhancing the healing of diabetic wounds by restoring the expression levels of TGF-β1, collagen-I, and α-SMA.
authors.affiliation: The Post-Professional DPT Program, The Richard Stockton College of New Jersey.
authors.forename: Tae Hoon
authors.initials: TH
authors.lastname: Kim
authors.forename: Hwi-Young
authors.initials: HY
authors.lastname: Cho
authors.forename: Suk Min
authors.initials: SM
authors.lastname: Lee
mesh_terms: D000199:Actins / Q000378:metabolism*; D000704:Analysis of Variance; D000818:Animals; D003094:Collagen / Q000378:metabolism*; D017931:DNA Primers / Q000235:genetics; D003921:Diabetes Mellitus, Experimental / Q000378:metabolism*; D004599:Electric Stimulation Therapy / Q000379:methods*; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley; D056910:Republic of Korea; D020133:Reverse Transcriptase Polymerase Chain Reaction; D053773:Transforming Growth Factor beta1 / Q000378:metabolism*; D014945:Wound Healing / Q000502:physiology*
chemical_list: D000199:Actins; D003094:Collagen; D017931:DNA Primers; D053773:Transforming Growth Factor beta1; C498862:Acta2 protein, rat