ABSTRACT
<p><b>OBJECTIVE</b>To investigate the epithelial growth factor (EGF) expression of EGF gene-transfected keratinocytes and its effect on cell proliferation after grafting.</p><p><b>METHODS</b>Newborn Balb/c mouse keratinocytes and gene transfected keratinocytes were seeded on the surface of acellular dermal matrix and cocultured in different ratios as follows: 1:1, 1:3, or 1:5 1 week after culture. The composite skin was grafted onto the full-thickness wound in Balb/c mouse. Specimen was harvested at interval after grafting and underwent the immunohistochemistry staining for EGF and proliferating cell nuclear antigen (PCNA).</p><p><b>RESULTS</b>Immunohistochemical staining showed EGF was expressed in the newly generated epidermis 1-2 week after grafting of the composite skin comprising Balb/c mouse keratinocytes and gene-transfected keratinocytes (at the ratio of 1:5). One week after surgery, Anti-PCNA positive basal cells were more than that in composite skin containing Balb/c mouse keratinocytes alone (P<0.01).</p><p><b>CONCLUSION</b>The gene-transfected keratinocytes expresses EGF and promotes the proliferation of keratinocytes in the early stage after transplantation.</p>
Subject(s)
Animals , Mice , Animals, Newborn , Cell Proliferation , Cells, Cultured , Coculture Techniques , Epidermal Growth Factor , Genetics , Keratinocytes , Cell Biology , Metabolism , Transplantation , Mice, Inbred BALB C , Skin , Wounds and Injuries , Skin Transplantation , Tissue Engineering , TransfectionABSTRACT
<p><b>OBJECTIVE</b>To investigate the role of p38 mitogen-activated protein kinase (MAPK) signal transduction pathway in the acute lung injury of severely burned rats.</p><p><b>METHODS</b>Forty-eight adult healthy rats were randomly divided into three groups: sham group, burn control group, and burn + SB203580 group. A third-degree burns over 30% total body surface area rat model was used and pulmonary capillary permeability, lung water content, pulmonary histology and p38 MAPK activity were measured at 24 hours postburn.</p><p><b>RESULTS</b>Burn trauma resulted in increased pulmonary capillary leakage permeability (42.5 +/- 4.7 vs. 12.1 +/- 1.4, P < 0.01), elevated lung water content (P < 0.05), and worsen histologic condition. There was a significant activation of p38 MAPK at 24 hours postburn compared with control. SB203580 inhibited the activation of p38 MAPK, reduced the pulmonary capillary leakage permeability (24.7 +/- 2.9 vs. 42.5 +/- 4.7, P < 0.01), decreased lung water content, and prevented burn-mediated lung injury.</p><p><b>CONCLUSION</b>The activation of p38 MAPK is one important aspect of the signaling event that contributes to burn-induced lung injury.</p>
Subject(s)
Animals , Male , Rats , Blotting, Western , Burns , Enzyme Activation , Enzyme Inhibitors , Pharmacology , Imidazoles , Pharmacology , Lung , Pathology , Mitogen-Activated Protein Kinases , Metabolism , Physiology , Pyridines , Pharmacology , Random Allocation , Rats, Sprague-Dawley , Respiratory Distress Syndrome , Signal Transduction , Physiology , p38 Mitogen-Activated Protein KinasesABSTRACT
<p><b>OBJECTIVE</b>To investigate the role of p38 mitogen-activated protein kinase (MAPK) signal transduction pathway in the production of the proinflammatory factors such as tumor necrosis factor (TNF-alpha) and interleukin 1beta (IL-1beta) in lungs and in the pulmonary endothelial cell injury in severely scalded rats.</p><p><b>METHODS</b>Forty eight adult healthy SD rats were randomly divided into three groups with 16 rats in each group, i.e. sham, burn and burn with SB203580 treatment groups. The changes in the TNF-alpha and IL-1beta contents in serum and bronchoalveolar lavage fluid (BALF), the von Willebrand factor (vWF) contents in plasma and pulmonary microvessels and pulmonary activating protein (AP-1) activity were determined at 24 postburn hours (PBH).</p><p><b>RESULTS</b>Compared with those in sham group, the TNF-alpha and IL-1beta contents in serum and BALF and the vWF content in plasma (194.2% +/- 28.3% vs 93.2% +/- 14.3%) at 24 PBH in burn group increased significantly (P < 0.01), whereas vWF content in pulmonary microvessel decreased obviously (1.1 +/- 0.3 vs 3.3 +/- 0.4, P < 0.01). In addition, the pulmonary AP-1 activity also increased at 24 PBH. Nevertheless, all the above indices improved obviously in burn with SB203580 (inhibitor of p38 MAPK signal transduction pathway) treatment group when compared with those in burn group.</p><p><b>CONCLUSION</b>AP-1 might mediate the production of proinflammatory factors, such as TNF-alpha and IL-1beta in lungs leading to pulmonary vascular endothelial injury, after being activated by activated p38 MAPK.</p>
Subject(s)
Animals , Male , Rats , Acute Lung Injury , Metabolism , Pathology , Burns , Metabolism , Pathology , Interleukin-1beta , Metabolism , Lung , Metabolism , Pathology , NF-kappa B , Metabolism , Rats, Sprague-Dawley , Signal Transduction , Tumor Necrosis Factor-alpha , Metabolism , p38 Mitogen-Activated Protein Kinases , MetabolismABSTRACT
<p><b>OBJECTIVE</b>To explore the relationship between the change in neuron specific enolase (NSE) and brain malfunction in burned patients.</p><p><b>METHODS</b>The serum samples of 11 burned patients with brain dysfunction were collected for the development of the serum level of neuron specific enolase with radioimmunoassay, and the correlation between condition of systemic inflammation and the levels of neuron specific enolase was assessed.</p><p><b>RESULTS</b>The level of NSE in burn patients with cerebral malfunction was obviously higher than that in control, and the level was correlated with the systemic inflammation.</p><p><b>CONCLUSION</b>The change in the level of serum NSE could reflect the damage degree of central nervous system to some extent.</p>