title: Transcutaneous electrical nerve stimulation (TENS) accelerates cutaneous wound healing and inhibits pro-inflammatory cytokines.
abstract: The purpose of this study was to evaluate transcutaneous electrical nerve stimulation (TENS) and other common treatment methods used in the process of wound healing in terms of the expression levels of pro-inflammatory cytokines. In the study, 24 female and 24 male adult Wistar-Albino rats were divided into five groups: (1) the non-wounded group having no incision wounds, (2) the control group having incision wounds, (3) the TENS (2 Hz, 15 min) group, (4) the physiological saline (PS) group and (5) the povidone iodine (PI) group. In the skin sections, interleukin-1 beta (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α) were assessed with enzyme-linked immunosorbent assay and immunohistochemical methods. In the non-wounded group, the expression of IL-1β, IL-6, and TNF-α signaling molecules was weaker in the whole tissue; however, in the control group, significant inflammatory response occurred, and strong cytokine expression was observed in the dermis, granulation tissue, hair follicles, and sebaceous glands (P < 0.05). In the TENS group, the decrease in TNF-α, IL-1β, and IL-6 immunoreaction in the skin was significant compared to the other forms of treatment (P < 0.05). Distinctive decreases of pro-inflammatory cytokines observed in the dermis in the TENS group suggest that TENS shortened the healing process by inhibating the inflammation phase.
authors.affiliation: Department of Histology and Embryology, School of Vocational Health Service, Celal Bayar University, Manisa, Turkey, serengurgen@gmail.com.
authors.forename: Seren Gülşen
authors.initials: SG
authors.lastname: Gürgen
authors.forename: Oya
authors.initials: O
authors.lastname: Sayın
authors.forename: Ferihan
authors.initials: F
authors.lastname: Cetin
authors.forename: Ayşe
authors.initials: A
authors.lastname: Tuç Yücel
mesh_terms: D000818:Animals; D016207:Cytokines / Q000037:antagonists & inhibitors* / Q000096:biosynthesis; D005260:Female; D007249:Inflammation / Q000276:immunology / Q000628:therapy*; D053583:Interleukin-1beta / Q000096:biosynthesis; D015850:Interleukin-6 / Q000096:biosynthesis; D008297:Male; D011206:Povidone-Iodine / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D012867:Skin / Q000293:injuries; D004561:Transcutaneous Electric Nerve Stimulation / Q000379:methods*; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis; D014945:Wound Healing / Q000502:physiology*
chemical_list: D016207:Cytokines; C000594089:IL1B protein, rat; D053583:Interleukin-1beta; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha; D011206:Povidone-Iodine