Abstract

The skin injury healing process involves the main phases of homoeostasis, inflammation, proliferation, and remodeling. The present study aimed to analyze the effects of low-level laser therapy (LLLT) on hematological dynamics, oxidative stress markers, and its relation with tissue healing following skin injury. Wistar rats were divided into control, sham, skin injury, and skin injury LLLT. The biochemical and morphological analyses were performed in the inflammatory (1 and 3 days) and regenerative phases (7, 14, and 21 days) following injury. The skin injury was performed in the dorsal region, between the intrascapular lines, using a surgical punch. LLLT (Al-Ga-In-P, λ=660 nm, energy density of 20 J/cm2, 30 mW power, and a time of 40 s) was applied at the area immediately after injury and on every following day according to the experimental subgroups. LLLT maintained hematocrit and hemoglobin levels until the 3rd day of treatment. Surprisingly, LLLT increased total leukocytes levels compared to control until the 3rd day. The effects of LLLT on mitochondrial activity were demonstrated by the significant increase in MTT levels in both inflammatory and regenerative phases (from the 1st to the 7th day), but only when associated with skin injury. The results indicated that LLLT modulated the inflammatory response intensity and accelerated skin tissue healing by a mechanism that involved oxidative damage reduction mostly at early stages of skin healing (inflammatory phase).

Highlights

  • Skin injuries, or ulcers, are commonly observed in all age groups, but mostly among older adults, those who are immobile and those with severe acute illness or neurological deficits [1]

  • A significant interaction was found in erythrocytes in the inflammatory phase for injury  level laser therapy (LLLT) (F(1, 6)=10.22, P=0.0187); Table 1 shows that neither injury nor treatment with LLLT caused a significant difference in erythrocyte count

  • LLLT was associated with increased leucocyte count on the first day compared to the Skin injury group (Po0.05, 95%CI=1.961 to 7.439)

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Summary

Introduction

Ulcers, are commonly observed in all age groups, but mostly among older adults, those who are immobile and those with severe acute illness or neurological deficits [1]. Skin injuries can contribute to further deterioration of one’s general health [2]. One of the most relevant physiological factors related to skin injury pathogenesis is the presence of vascular dysfunction – such as chronic venous insufficiency and/or peripheral arterial occlusive diseases – and sustained hyperglycemia [4]. It is widely accepted that ischemia is a primary factor involved in skin injury genesis and evolution, but it is the blood reflow to ischemic areas that accelerates cell death due to an overproduction of reactive oxygen species (ROS). An increase in ROS levels that exceeds the antioxidant defenses of the skin leads to impairments in cellular biomolecular functions via a mechanism known as oxidative stress [7]

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