Respostas celulares do fígado e do músculo esquelético distante da lesão térmica corporal em ratos wistar jovens

• Ano de defesa: 2014
• Autor(a) principal: Bortolin, Jeferson André [UNIFESP]
• Tipo de documento: Dissertação
• Tipo de acesso: Acesso aberto
• Idioma: por
• Instituição de defesa: Universidade Federal de São Paulo (UNIFESP)
• Palavras-chave em Português: Burns; Skeletal muscle; Liver; Immunohistochemistry and transmission electron microscopy; Queimaduras; Músculo esquelético; Fígado; Imunoistoquímica; Microscopia eletrônica de transmissão
• Link de acesso: https://sucupira.capes.gov.br/sucupira/public/consultas/coleta/trabalhoConclusao/viewTrabalhoConclusao.jsf?popup=true&id_trabalho=519984; https://repositorio.unifesp.br/handle/11600/46375

Introduction: Thermal Injuries represent a public health problem and is a major cause of accidents in children and adolescents. The most obvious feature of thermal injuries corresponds to extensive tissue destruction, leading to activation of catabolic processes in the body. Purpose: The aim of this study is to understand the cellular mechanisms related to the systemic effects of thermal scald injury in the liver and skeletal muscle distant from the injury. Methods: 42 young rats were used equally divided into the following groups: control (CTRL) and scalding burn injury (SBI). SBI is 45% of the body surface and euthanasia of the animals occurred at 1, 4 and 14 days after injury. After this period has been removed the middle part of the medial gastrocnemius muscle and liver fragment. The liver samples were subjected to histological analysis (hematoxylin & eosin and Sirius red), immunohistochemistry of inflammatory mediator cyclooxygenase-2 (COX-2), Polymerase Chain Reaction in Real Time (qPCR) of the inflammatory mediators tumor necrosis factor alpha (TNF-α), nitric oxide synthase (iNOS), COX-2 and cell apoptosis effector caspase-3. Have samples of skeletal muscle were subjected to ultrastructural analysis by transmission electron microscopy (TEM). Results: Histopathology showed change in radial alignment of hepatocytes in relation to the vessel, increased sinusoidal space and size disuniform hepatocyte morphology of the liver in animals subjected to SBI. The identification of collagen staining with Sirius Red (SR) has been demonstrated focal accumulation of connective tissue (collagen type III) in the liver 14 days after the SBI. Immunohistochemical labeling for COX-2 was evidenced focal immunoblots in the livers of animals with SBI and decreasing with the experimental days. Analysis of qPCR for inflammatory mediators (TNF-α, COX-2 and iNOS) and the effector of apoptosis, caspase-3, there was no significant difference between groups. Regarding the ultrastructural analysis of the striated skeletal muscle was evidenced accumulation of lipid bodies (related to inflammation) and degeneration of myofibrils with fragmentation of Z lines in animals that underwent SBI. Regarding quantitative results evidenced a decrease in body mass and an increase in the area of the hepatocytes of animals with 14 after SBI. In mononuclear cell density of hepatocytes and sinusoidal cells binucleate significant difference in the groups and the time of the experiment and compared to gene expression of proteins there were no significant changes between groups. Conclusion: We conclude that the body thermal injury to great extent has systemic effects, triggering the activation of cellular responses such as: changes in structural morphology of liver tissue, ultrastructural changes in skeletal muscle morphology, inflammation of the liver tissue and accumulation of tissue connective liver and skeletal muscle far from the lesion. With the understanding of the mechanisms investigated, this work may contribute to the establishment of effective rehabilitation strategies in large burns.