Oxidative stress is involved in LLLT mechanism of action on skin healing in rats.

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).