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; (3) LASER-20 was animals treated with intraperitoneal saline solution and exposed to an infrared laser at 20 J cm; (4) acute lung injury (ALI) was animals treated with intraperitoneal LPS (10 mg kg); (5) ALI-LASER10 was animals treated with intraperitoneal LPS (10 mg kg) and, after 4 h, exposed to an infrared laser at 10 J cm and (6) ALI-LASER20 was animals treated with intraperitoneal LPS (10 mg kg) and, after 4 h, exposed to an infrared laser at 20 J cm. Irradiation was performed only once and animal euthanasias for analysis of mRNA relative levels by RT-qPCR.

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.

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.

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.

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.

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.

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.

L-NAME and L-arginine differentially ameliorate cigarette smoke-induced emphysema in mice.

Nitric oxide (NO) represents one of the most important intra- and extracellular mediators and takes part in both biologic and pathologic processes. This study aimed to verify the treatment with an NO inhibitor and an NO substrate in pulmonary emphysema induced by cigarette smoke (CS) in a murine model. We compared N-acetylcysteine (NAC), a precursor of glutathione, to G-nitro-L-arginine-methyl ester or L-NAME (LN), which is an NO inhibitor, and to l-arginine (LA), which is a substrate for NO formation.