Low-power infrared laser modulates mRNA levels from genes of base excision repair and genomic stabilization in heart tissue from an experimental model of acute lung injury.

The aim of this study was to evaluate photobiomodulation effects on mRNA relative levels from genes of base excision repair and genomic stabilization in heart tissue from an experimental model of acute lung injury by sepsis. For experimental procedure, animals were randomly assigned to six main groups: (1) control group was animals treated with intraperitoneal saline solution; (2) LASER-10 was animals treated with intraperitoneal saline solution and exposed to an infrared laser at 10 J cm-2; (3) LASER-20 was animals treated with intraperitoneal saline solution and exposed to an infrared laser at 20 J cm-2; (4) acute lung injury (ALI) was animals treated with intraperitoneal LPS (10 mg kg-1); (5) ALI-LASER10 was animals treated with intraperitoneal LPS (10 mg kg-1) and, after 4 h, exposed to an infrared laser at 10 J cm-2 and (6) ALI-LASER20 was animals treated with intraperitoneal LPS (10 mg kg-1) and, after 4 h, exposed to an infrared laser at 20 J cm-2. Irradiation was performed only once and animal euthanasias for analysis of mRNA relative levels by RT-qPCR. Our results showed that there was a reduction of mRNA relative levels from ATM gene and an increase of mRNA relative levels from P53 gene in the heart of animals with ALI when compared to the control group. In addition, there was an increase of mRNA relative levels from OGG1 and APE1 gene in hearts from animals with ALI when compared to the control group. After irradiation, an increase of mRNA relative levels from ATM and OGG1 gene was observed at 20 J cm-2. In conclusion, low-power laser modulates the mRNA relative levels from genes of base excision repair and genomic stabilization in the experimental model of acute lung injury evaluated.

Low-power infrared laser modulates telomere length in heart tissue from an experimental model of acute lung injury.

Acute lung injury and acute respiratory distress syndrome can occur as a result of sepsis. Cardiac dysfunction is a serious component of multi-organ failure caused by severe sepsis. Telomere shortening is related to several heart diseases. Telomeres are associated with the shelterin protein complex, which contributes to the maintenance of telomere length. Low-power infrared lasers modulate mRNA levels of shelterin complex genes. This study aimed to evaluate effects of a low-power infrared laser on mRNA relative levels of genes involved in telomere stabilization and telomere length in heart tissue of an experimental model of acute lung injury caused by sepsis. Animals were divided into six groups, treated with intraperitoneal saline solution, saline solution and exposed to a low-power infrared laser at 10 J cm-2 and 20 J cm-2, lipopolysaccharide (LPS), and LPS and, after 4 h, exposed to a low-power infrared laser at 10 J cm-2 and 20 J cm-2. The laser exposure was performed only once. Analysis of mRNA relative levels and telomere length by RT-qPCR was performed. Telomere shortening and reduction in mRNA relative levels of TRF1 mRNA in heart tissues of LPS-induced ALI animals were observed. In addition, laser exposure increased the telomere length at 10 J cm-2 and modulated the TRF1 mRNA relative levels of at 20 J cm-2 in healthy animals. Although the telomeres were shortened and mRNA levels of TRF1 gene were increased in nontreated controls, the low-power infrared laser irradiation increased the telomere length at 10 J cm-2 in cardiac tissue of animals affected by LPS-induced acute lung injury, which suggests that telomere maintenance is a part of the photobiomodulation effect induced by infrared radiation.

Heat delays skin wound healing in mice.

In vivo studies have shown that the combination of infrared radiation (IR) and visible light (VIS) is responsible for the activation of metaloproteinases, causing matrix degradation and damage to healthy skin. However, the role of heat originating from the VIS spectrum on wound healing remains poorly understood. Our objective was to investigate the macroscopic, microscopic and biochemical effects of heat induced by visible light on cutaneous wound healing in mice. Male mice were anesthetized, subjected to a cutaneous excisional wound and divided into two groups ( n = 10/group) exposed to 23℃ or 43℃ in a thermal chamber for 30 min every other day, for 13 days. On day 14, the animals were sacrificed, and their lesions were processed for histochemistry, immunohistochemistry and protein expression analysis. The wound area was 42% greater 11 days ( p < 0.01) and 29% greater 14 days ( p < 0.001) after wounding in the 43℃ group than in the 23℃ group. The 43℃ group presented a lower (17%) percentage of reepithelialized wounds ( p < 0.001) 14 days after wounding. The length of the epidermal gap was greater in the 43℃ group ( p < 0.01). The volume density of myofibroblasts and the number of F4/80-positive macrophages was greater in the 43℃ group ( p < 0.05). The 43℃ group showed increased protein expression of type III collagen ( p < 0.001), decreased protein expression of type I collagen ( p < 0.05), increased MMP-1 expression ( p < 0.05), and decreased MMP-2 activity ( p < 0.001). The protein expression of fibrillin-1 ( p < 0.001), MMP-12 ( p < 0.05), TGF-ß 1/2/3 ( p < 0.01) and ERK activation ( p < 0.05) was increased in the 43℃ group. Our results suggest that heat delays the stages of wound healing in mice.

Low-level red laser improves healing of second-degree burn when applied during proliferative phase.

The aim of this study was to investigate the effects of low-level red laser on tissue repair in rats submitted to second-degree burn, evaluating if the timing of laser treatment influences the healing process. The animals had their backs shaved and divided as follows: control group (n = 12)-rats burned and not irradiated, early laser group (n = 12)-rats burned and irradiated from day 1 after injury for five consecutive days, and late laser group (n = 14)-rats burned and irradiated from day 4 after injury for five consecutive days. Laser irradiation was according to a clinical protocol (20 J/cm(2), 100 mW, continuous wave emission mode, 660 nm) as recommended by the laser device manufacturer. Half of the animals were sacrificed 10 days after burn, and the other animals were sacrificed 21 days after burn. The late laser group accelerated wound contraction 10 and 21 days after burn. The late laser group accelerated reepithelialization 18 days after burn. The late laser group increases the granulation tissue 10 and 21 days after burn. Both irradiated groups increased type III collagen expression and TGF-ß 21 days after burn. Both irradiated groups increased macrophage and myofibroblast numbers 10 days after burn and decreased 21 days after. Low-level red laser exposure contributes to the process of tissue repair of second-degree burns, but the intervention during proliferative phase is crucial in the final outcome of the repair process.