ABSTRACT
OBJECTIVE@#To establish the model of skin scald in mice for the study of skin thermal injuries.@*METHODS@#After anaesthetization mice were scalded in a 1 cm-diameter circle area on the central dorsum by boiling water at contact times: 10s or 25s. The mice were sacrificed at 1, 3, 5, 7 and 10 days after scald. The skin samples were collected and analyzed by gross and histopathological examinations.@*RESULTS@#Deep II degree thermal injury involving full-thickness skin was observed in the 10s scald group. III degree thermal injury involving full-thickness skin and the dorsal skeletal muscle was observed in the 25 s scald group.@*CONCLUSION@#A mouse skin scald model is established which is stable and can be used on the skin thermal injury in future research.
Subject(s)
Animals , Female , Male , Mice , Burns/pathology , Disease Models, Animal , Epithelium/pathology , Hot Temperature/adverse effects , Random Allocation , Reproducibility of Results , Severity of Illness Index , Skin/pathology , Time FactorsABSTRACT
OBJECTION@#To investigate the time-dependent appearance of circulating fibrocytes of skeletal muscle in rats after contusion.@*METHODS@#The model of skeletal muscle wound was established in rat. The circulating fibrocytes in contused skeletal muscle were detected by CD45 and procollagen I double immunofluorescence staining method.@*RESULTS@#In the control group, CD45- and procollagen I-positive cells were not detected in skeletal muscle. A few CD45 cells were observed aged from 6 h to 1 d after contusion. A few CD45- and procollagen I-positive cells (fibrocytes) initially gathered in injury area 3d after injury. The ratio of positive fibrocytes significantly increased 5 d after injury. The ratio of fibrocytes was highest at 7 d after contusion and then decreased. The volume of fibrocytes showed bigger with injury time increase compared with 3 d group. The expression of procollagen I and CD45 were weakened at 14d after injury.@*CONCLUSION@#The circulating fibrocytes are detected in contused skeletal muscle in time-dependent pattern. Circulating fibrocytes may be a marker in the wound age determination for contused skeletal muscle.
Subject(s)
Animals , Male , Rats , Biomarkers/metabolism , Collagen Type I/metabolism , Contusions/pathology , Disease Models, Animal , Forensic Pathology , Immunohistochemistry , Leukocyte Common Antigens/metabolism , Mesenchymal Stem Cells/metabolism , Microscopy, Fluorescence , Muscle, Skeletal/pathology , Random Allocation , Rats, Sprague-Dawley , Time Factors , Wound HealingABSTRACT
<p><b>OBJECTIVE</b>To explore the effects and related mechanism of nifedipine on vascular inflammation induced by cuff placement.</p><p><b>METHODS</b>Adult male C57BL/6J mice (10 to 12 weeks of age) were assigned to control (no cuff placement without nifedipine), cuff placement (cuff placement without nifedipine) and treatment (cuff placement with nifedipine 1 or 5 mg×kg(-1)×d(-1)) groups. Activity of NF-κB in injured artery was measured 5 days after operation. MCP-1 expression and nuclear translocation of NF-κB were examined in injured artery 7 days after operation.</p><p><b>RESULTS</b>DNA-binding activity of NF-κB was significantly increased in the injured artery 5 days after cuff placement which could be downregulated by nifedipine 5 mg×kg(-1)×d(-1). MCP-1 mRNA expression in the injured arteries was increased 7 days after cuff placement and which could be significantly attenuated by nifedipine 5 mg×kg(-1)×d(-1). Cuff placement decreased the cytoplasmic level of p50, IκBα, IκBβ, and increased the nuclear level of p50. Nifedipine 5 mg×kg(-1)×d(-1) significantly attenuated these changes.</p><p><b>CONCLUSION</b>Our results suggest that high dose nifedipine could suppresses expression of MCP-1 induced by injured arteries via the inhibin NF-κB DNA binding activity, thereby attenuating vascular inflammation.</p>