RU486 improves cutaneous wound healing in mice submitted to psychological stress

Abstract

Cutaneous wound healing is a complex process involving inflammation, granulation tissue formation, and remodeling, which result in scar formation. Chronic stress impairs cutaneous wound healing through the activation of the hypothalamic–pituitary– adrenal axis (HPA). Among the products of HPA are glucocorticosteroid (GC) hormones, which have been shown to delay wound closure. Therefore, we evaluate the effects of administration of a GC receptor antagonist (RU486) on cutaneous wound healing of chronically stressed mice. Male mice were stressed by spun at 115 rpm for 15 min per hour, daily, until euthanasia. A group of mice were only chronically stressed. A group of chronically stressed mice received daily I.P. injection of RU486 (20mg/Kg). Control mice were not subjected to stress, but received RU486 daily. An excisional lesion was made and measured. Fourteen days later, mice were killed to collect blood and lesions. The inflammatory infiltrate, angiogenesis, mieloperoxidase (MPO), and collagen deposition were evaluated in wounds. Stressed RU486‐treated mice showed a worst rate of contraction and re‐epithelialization than RU486‐treated controls. Stressed RU486‐treated mice demonstrate a recovery of MPO activity when compared to stressed animals. Our preliminary results indicate that blocking GC signalization improve wound healing in stressed mice. Supported by CAPES, FAPERJ & CNPq.