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.

The oxidative response of mouse hearts is modulated by genetic background.

BACKGROUND: Smoking plays an important role in cardiovascular diseases. However, the reasons why some individuals develop those diseases and others do not remain to be explained. OBJECTIVE: This study aimed at assessing the redox profile of the heart of different mouse strains after exposure to cigarette smoke. METHODS: Male mice of the Swiss (n = 10), C3H (n = 10), BALB/c (n = 10) and C57BL/6 (n = 10) strains were exposed to cigarette smoke (12 cigarettes/day), while their respective controls (n = 10) were exposed to ambient air for 60 days. After being euthanized, their heart was removed for biochemical analyses. RESULTS: Although the malondialdehyde content did not increase in any of the groups, catalase activity decreased in the Swiss (p < 0.05) and BALB/c (p < 0.05) strain mice as compared with their respective control groups, while myeloperoxidase decreased in the C3H (p < 0.05) and C57BL/6 (p < 0.001) strain mice as compared with their respective control groups. The reduced glutathione content decreased in the Swiss, C3H, C57BL/6 (p < 0.05) and BALB/c (p < 0,001) strain mice as compared with their respective control groups. Regarding reduced glutathione content, an increase was observed in the Swiss strain mice (p < 0.05), while a decrease was observed in the C3H (p < 0.05) and BALB/c (p < 0.001) strain mice as compared with their respective control groups. The reduced glutathione/reduced glutathione ratio showed a reduction in the Swiss and C57BL/6 (p < 0.05) strain mice as compared with their respective control groups. CONCLUSIONS: The genetic background of mice can influence the antioxidant response after exposure to cigarette smoke and seems to be a determinant factor for redox imbalance in Swiss and C57BL/6 strain mice. Understanding antioxidant responses and genetic background of C3H and BALB/c strain mice might provide important information regarding cardiac resistance to cigarette smoke.

A resposta oxidativa em corações de camundongos é modulada por background genético / The oxidative response of mouse hearts is modulated by genetic background

FUNDAMENTO: o tabagismo apresenta importante papel sobre as doenças cardiovasculares, entretanto permanecem pouco compreendidos os motivos pelos quais alguns seres humanos as desenvolvem e outros não. OBJETIVO: nosso objetivo foi analisar o perfil redox do coração de diferentes linhagens de camundongos após exposição à fumaça de cigarro. MÉTODOS: camundongos machos suíços (n = 10), C3H (n = 10), BALB/c (n = 10) e C57BL/6 (n = 10) foram expostos à fumaça de cigarro (12 cigarros/dia), enquanto os respectivos controles (n = 10) ao ar ambiente por 60 dias. Após sacrifício, o coração foi retirado para análises bioquímicas. RESULTADOS: embora o conteúdo de malondialdeído não tenha aumentado em nenhum grupo, a atividade da catalase diminuiu no grupo suíço (p < 0,05), BALB/c (p < 0,05) quando comparados aos respectivos grupos-controle, enquanto a mieloperoxidase diminuiu no grupo C3H (p < 0,05) e C57BL/6 (p < 0,001) quando comparados aos respectivos grupos controle. O conteúdo de glutationa reduzida diminuiu nos grupos suíço, C3H, C57BL/6 (p < 0,05) e no grupo BALB/c (p < 0,001) quando comparados com os respectivos controles. Observamos aumento do conteúdo da glutationa oxidada no grupo Suíço (p < 0,05) e diminuição nos grupos C3H (p < 0,05) e BALB/c (p < 0,001) quando comparados aos respectivos grupos-controle. A razão glutationa reduzida/ glutationa oxidada apresentou redução nos grupos suíço e C57BL/6 (p < 0.05) quando comparados aos grupos controle. CONCLUSÃO: o background genético nos camundongos pode influenciar na resposta antioxidante após a exposição à fumaça de cigarro e parece ser um fator determinante para o desequilíbrio redox no suíço e C57BL/6. Compreender as respostas antioxidantes e do background genético C3H e BALB/c podem fornecer importantes informações quanto à resistência cardíaca a fumaça de cigarro.

BACKGROUND: Smoking plays an important role in cardiovascular diseases. However, the reasons why some individuals develop those diseases and others do not remain to be explained. OBJECTIVE: This study aimed at assessing the redox profile of the heart of different mouse strains after exposure to cigarette smoke. METHODS: Male mice of the Swiss (n = 10), C3H (n = 10), BALB/c (n = 10) and C57BL/6 (n = 10) strains were exposed to cigarette smoke (12 cigarettes/day), while their respective controls (n = 10) were exposed to ambient air for 60 days. After being euthanized, their heart was removed for biochemical analyses. RESULTS: Although the malondialdehyde content did not increase in any of the groups, catalase activity decreased in the Swiss (p < 0.05) and BALB/c (p < 0.05) strain mice as compared with their respective control groups, while myeloperoxidase decreased in the C3H (p < 0.05) and C57BL/6 (p < 0.001) strain mice as compared with their respective control groups. The reduced glutathione content decreased in the Swiss, C3H, C57BL/6 (p < 0.05) and BALB/c (p < 0,001) strain mice as compared with their respective control groups. Regarding reduced glutathione content, an increase was observed in the Swiss strain mice (p < 0.05), while a decrease was observed in the C3H (p < 0.05) and BALB/c (p < 0.001) strain mice as compared with their respective control groups. The reduced glutathione/reduced glutathione ratio showed a reduction in the Swiss and C57BL/6 (p < 0.05) strain mice as compared with their respective control groups. CONCLUSIONS: The genetic background of mice can influence the antioxidant response after exposure to cigarette smoke and seems to be a determinant factor for redox imbalance in Swiss and C57BL/6 strain mice. Understanding antioxidant responses and genetic background of C3H and BALB/c strain mice might provide important information regarding cardiac resistance to cigarette smoke.

Redox imbalance and pulmonary function in bleomycin-induced fibrosis in C57BL/6, DBA/2, and BALB/c mice.

The development of bleomycin-induced pulmonary fibrosis (BLEO-PF) has been associated with differences in genetic background and oxidative stress status. The authors' aim was to investigate the crosstalk between the redox profile, lung histology, and respiratory function in BLEO-PF in C57BL/6, DBA/2, and BALB/c mice. BLEO-PF was induced with a single intratracheal dose of bleomycin (0.1 U/mouse). Twenty-one days after bleomycin administration, the mortality rate was over 50% in C57BL/6 and 20% in DBA/2 mice, and BLEO-PF was not observed in BALB/c. There was an increase in lung static elastance (p < .001), viscoelastic/inhomogeneous pressure (p < .05), total pressure drop after flow interruption (p < .01), and ΔE (p < .05) in C57BL/6 mice. The septa volume increased in C57BL/6 (p < .05) and DBA/2 (p < .001). The levels of IFN-γ were reduced in C57BL/6 mice (p < .01). OH-proline levels were increased in C57BL/6 and DBA/2 mice (p < .05). SOD activity and expression were reduced in C57BL/6 and DBA/2 mice (p < .001 and p < .001, respectively), whereas catalase was reduced in all strains 21 days following bleomycin administration compared with the saline groups (C57BL/6: p < .05; DBA/2: p < .01; BALB/c: p < .01). GPx activity and GPx1/2 expression decreased in C57BL/6 (p < .001). The authors conclude that BLEO-PF resistance may also be related to the activity and expression of SOD in BALB/c mice.

Endotoxin-induced acute lung injury is dependent upon oxidative response.

The aim of the present study was to investigate the involvement of oxidative stress in acute lung injury (ALI) induced by lipopolysaccharide (LPS) and its effects upon cell structure, function and inflammation. In total, 108 male C57BL/6 mice were divided into seven groups: CTR Group (50 µL of saline) administered intratracheally (i.t.), LPS 6 h (10 µg of LPS - i.t.), LPS 12 h (10 µg of LPS - i.t.), LPS 24 h (10 µg of LPS - i.t.), LPS 48 h (10 µg of LPS - i.t.), LPS 24 h (10 µg - i.t.) + NAC 40 mg/kg (gavage) and 24 h LPS (10 µg - i.t.) + NAC 100 mg/kg (gavage). The antioxidant treatment protected the lungs from stress in the first 12 h, but significant oxidative stress induction was observed at the 24-hour time point, and, after 48 h, there was no protection exerted by the antioxidant treatment. NAC (N-acetylcysteine) reversed the elastance parameters, and ΔP1 and ΔP2 compared with 24 h LPS alone. NAC reduced the number of inflammatory cells in histology analysis when compared with the 24 h LPS alone-treated group. NAC also inhibited the transcription of NFκB, IL-6, TNF-α and COX2 usually induced by LPS. Our results suggest that oxidative stress plays an important role in structural, functional and inflammatory responses in the ALI model.